Fatty Acid Metabolism in Health and Cancer: From Fundamental Mechanisms to Therapeutic Application

Na Hang , Runkang Zhao , Fan Zhang , Dandan Guo , Qing Li , Zhijun Shen , Ruiqing Gao , Chenyu Gao , Zhao Xie , Sentao Fu , Peng Luo , Bufu Tang , Ling Wang

MedComm ›› 2026, Vol. 7 ›› Issue (6) : e70749

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MedComm ›› 2026, Vol. 7 ›› Issue (6) :e70749 DOI: 10.1002/mco2.70749
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Fatty Acid Metabolism in Health and Cancer: From Fundamental Mechanisms to Therapeutic Application
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Abstract

Fatty acid metabolism (FAM) plays a vital role in maintaining health by supporting energy production, cellular structure, and signaling processes. However, once this tightly regulated network becomes disrupted, it is increasingly recognized as being linked to the onset and progression of numerous chronic diseases, with cancer being one of the most prominent and clearly defined examples. In addition to the field of oncology, alterations in FAM can also lead to immune dysfunction, inflammatory responses, and metabolic disorders, including diabetes, cardiovascular disease, and neurodegenerative diseases. We examine how different cell types adapt their metabolic behavior within inflamed and tumor-rich environments, often leveraging FAM to support survival or suppress immune activity. By highlighting recent discoveries in metabolic regulation, intercellular communication, and disease-specific lipid signatures, we identify new opportunities for therapeutic intervention. These include targeted drugs, gene therapies, nanomedicine platforms, and dietary strategies aimed at restoring metabolic balance. We also discuss the emerging role of fatty acid-related biomarkers in advancing precision oncology and broader applications in personalized medicine. Together, these insights underscore the centrality of FAM in human health and disease, with particular emphasis on its growing promise as a therapeutic target in cancer and beyond.

Keywords

fatty acid metabolism / inflammatory microenvironment / metabolic reprogramming / targeted therapy / tumor microenvironment

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Na Hang, Runkang Zhao, Fan Zhang, Dandan Guo, Qing Li, Zhijun Shen, Ruiqing Gao, Chenyu Gao, Zhao Xie, Sentao Fu, Peng Luo, Bufu Tang, Ling Wang. Fatty Acid Metabolism in Health and Cancer: From Fundamental Mechanisms to Therapeutic Application. MedComm, 2026, 7 (6) : e70749 DOI:10.1002/mco2.70749

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References

[1]

P. Morigny, J. Boucher, P. Arner, and D. Langin, “Lipid and Glucose Metabolism in White Adipocytes: Pathways, Dysfunction and Therapeutics,” Nature Reviews Endocrinology 17, no. 5 (2021): 276–295.

[2]

A. J. Mathiowetz and J. A. Olzmann, “Lipid Droplets and Cellular Lipid Flux,” Nature Cell Biology 26, no. 3 (2024): 331–345.

[3]

S. Casagrande and G. Dell'Omo, “Linking Warmer Nest Temperatures to Reduced Body Size in Seabird Nestlings: Possible Mitochondrial Bioenergetic and Proteomic Mechanisms,” Journal of Experimental Biology 228, no. 6 (2025): jeb249880.

[4]

E. Asadollahi, A. Trevisiol, A. S. Saab, et al., “Oligodendroglial Fatty Acid Metabolism as a Central Nervous System Energy Reserve,” Nature Neuroscience 27, no. 10 (2024): 1934–1944.

[5]

A. Sakers, M. K. De Siqueira, P. Seale, and C. J. Villanueva, “Adipose-tissue Plasticity in Health and Disease,” Cell 185, no. 3 (2022): 419–446.

[6]

T. Bo, L. Gao, Z. Yao, et al., “Hepatic Selective Insulin Resistance at the Intersection of Insulin Signaling and Metabolic Dysfunction-associated Steatotic Liver Disease,” Cell Metabolism 36, no. 5 (2024): 947–968.

[7]

V. D. Dahik, P. Kc, C. Materne, et al., “ABCG1 orchestrates Adipose Tissue Macrophage Plasticity and Insulin Resistance in Obesity by Rewiring Saturated Fatty Acid Pools,” Science Translational Medicine 16, no. 777 (2024): eadi6682.

[8]

H. Cao, K. Gerhold, J. R. Mayers, M. M. Wiest, S. M. Watkins, and G. S. Hotamisligil, “Identification of a Lipokine, a Lipid Hormone Linking Adipose Tissue to Systemic Metabolism,” Cell 134, no. 6 (2008): 933–944.

[9]

J. L. M. Björkegren and A. J. Lusis, “Atherosclerosis: Recent Developments,” Cell 185, no. 10 (2022): 1630–1645.

[10]

A. Ray, P. Alabarse, R. Malik, et al., “Single-cell Transcriptome-wide Mendelian Randomization and Colocalization Analyses Uncover Cell-specific Mechanisms in Atherosclerotic Cardiovascular Disease,” American Journal of Human Genetics 112, no. 7 (2025): 1597–1609.

[11]

J. Zhang, F. Ouyang, A. Gao, et al., “ESM1 enhances Fatty Acid Synthesis and Vascular Mimicry in Ovarian Cancer by Utilizing the PKM2-dependent Warburg Effect Within the Hypoxic Tumor Microenvironment,” Molecular Cancer 23, no. 1 (2024): 94.

[12]

Z. Chen, Y. Gong, F. Chen, et al., “Orchestrated Desaturation Reprogramming From Stearoyl-CoA Desaturase to Fatty Acid Desaturase 2 in Cancer Epithelial-mesenchymal Transition and Metastasis,” Cancer Commun Lond Engl 45, no. 3 (2025): 245–280.

[13]

W. Liu, Z. Wang, Z. Li, et al., “Lipid Metabolic Reprogramming in the Tumor Microenvironment and Its Mechanistic Role in Immunosuppressive Cells,” Frontiers in Immunology 16 (2025): 1728354.

[14]

R. Jin, L. Neufeld, and T. L. McGaha, “Linking Macrophage Metabolism to Function in the Tumor Microenvironment,” Nat Cancer 6, no. 2 (2025): 239–252.

[15]

S. Sung, H. J. Kim, S. J. Cha, M. Nahm, S. H. Kim, and M. S. Kwon, “Microglial Lipid Droplets as Therapeutic Targets in Age-Related Neurodegenerative Diseases,” Npj Aging (2025), Published online November 30.

[16]

Q. Liu, Y. Kong, H. Kang, Y. Jiang, and X. Hao, “Circulating Polyunsaturated Fatty Acids Percentages and Coronary Artery Disease Incidence and Mortality: Observational and Mendelian Randomization Analyses,” Clinical Nutrition Edinburgh Scotland 48 (2025): 122–133.

[17]

B. Liu, R. Liu, Y. Gu, X. Shen, J. Zhou, and C. Luo, “Polyunsaturated Fatty Acids and Diabetic Microvascular Complications: A Mendelian Randomization Study,” Front Endocrinol 15 (2024): 1406382.

[18]

T. Zhou, J. Cheng, S. He, et al., “The Sphingosine-1-phosphate Receptor 1 Mediates the Atheroprotective Effect of Eicosapentaenoic Acid,” Nature Metabolism 6, no. 8 (2024): 1566–1583.

[19]

X. Xu, H. Li, H. Lin, et al., “MIF-Mediated Crosstalk Between THRSP + Hepatocytes and CD74 + Lipid-Associated Macrophages in Hepatic Periportal Zone Drives MASH,” Hepatol Baltim Md (2025), Published online June 12.

[20]

A. Rai, K. Huynh, J. Cross, et al., “Multi-omics Identify Hallmark Protein and Lipid Features of Small Extracellular Vesicles Circulating in human Plasma,” Nature Cell Biology 27, no. 12 (2025): 2167–2185.

[21]

I. Trujillo-Gonzalez, P. G. Thomes, I. T. Sakallioglu, and K. K. Kharbanda, “Editorial: Leveraging Multi-omics Approaches to Understand and Manage Gastrointestinal and Hepatic Diseases,” Frontiers in pharmacology 15 (2024): 1529088.

[22]

S. J. Wakil and L. A. Abu-Elheiga, “Fatty Acid Metabolism: Target for Metabolic Syndrome,” Journal of Lipid Research 50, no. Suppl (2009): S138–143.

[23]

M. T. Snaebjornsson, S. Janaki-Raman, and A. Schulze, “Greasing the Wheels of the Cancer Machine: The Role of Lipid Metabolism in Cancer,” Cell Metabolism 31, no. 1 (2020): 62–76.

[24]

C. R. Santos and A. Schulze, “Lipid Metabolism in Cancer,” Federation of European Biochemical Societies Journal 279, no. 15 (2012): 2610–2623.

[25]

F. Röhrig and A. Schulze, “The Multifaceted Roles of Fatty Acid Synthesis in Cancer,” Nature Reviews Cancer 16, no. 11 (2016): 732–749.

[26]

M. Bacci, N. Lorito, A. Smiriglia, and A. Morandi, “Fat and Furious: Lipid Metabolism in Antitumoral Therapy Response and Resistance,” Trends in Cancer 7, no. 3 (2021): 198–213.

[27]

A. J. Hoy, S. R. Nagarajan, and L. M. Butler, “Tumour Fatty Acid Metabolism in the Context of Therapy Resistance and Obesity,” Nature Reviews Cancer 21, no. 12 (2021): 753–766.

[28]

Q. Qu, F. Zeng, X. Liu, Q. J. Wang, and F. Deng, “Fatty Acid Oxidation and Carnitine Palmitoyltransferase I: Emerging Therapeutic Targets in Cancer,” Cell Death & Disease 7, no. 5 (2016): e2226.

[29]

S. M. Houten, S. Violante, F. V. Ventura, and R. J. A. Wanders, “The Biochemistry and Physiology of Mitochondrial Fatty Acid β-Oxidation and Its Genetic Disorders,” Annual Review of Physiology 78 (2016): 23–44.

[30]

Y. Ma, S. M. Temkin, A. M. Hawkridge, et al., “Fatty Acid Oxidation: An Emerging Facet of Metabolic Transformation in Cancer,” Cancer Letters 435 (2018): 92–100.

[31]

J. Plutzky, “Expansion and Contraction: The Mighty, Mighty Fatty Acid,” Nature Medicine 15, no. 6 (2009): 618–619.

[32]

S. Jin, N. A. Yoon, M. Wei, et al., “Endoplasmic Reticulum Nogo Drives AgRP Neuronal Activation and Feeding Behavior,” Cell Metabolism 37, no. 6 (2025): 1400–1412.e8.

[33]

Q. Wang, B. Zhang, B. Stutz, Z. W. Liu, T. L. Horvath, and X. Yang, “Ventromedial Hypothalamic OGT Drives Adipose Tissue Lipolysis and Curbs Obesity,” Science Advances 8, no. 35 (2022): eabn8092.

[34]

J. W. Park, S. E. Park, W. Koh, et al., “Hypothalamic Astrocyte NAD+ Salvage Pathway Mediates the Coupling of Dietary Fat Overconsumption in a Mouse Model of Obesity,” Nature Communications 15, no. 1 (2024): 2102.

[35]

K. Tokizane, C. S. Brace, and S. I. Imai, “DMHPpp1r17 neurons Regulate Aging and Lifespan in Mice Through Hypothalamic-adipose Inter-tissue Communication,” Cell Metabolism 36, no. 2 (2024): 377–392.e11.

[36]

P. Hammerschmidt, S. M. Steculorum, C. L. Bandet, et al., “CerS6-dependent Ceramide Synthesis in Hypothalamic Neurons Promotes ER/Mitochondrial Stress and Impairs Glucose Homeostasis in Obese Mice,” Nature Communications 14, no. 1 (2023): 7824.

[37]

S. Ouyang, S. Xiang, X. Wang, et al., “The Downregulation of SCGN Induced by Lipotoxicity Promotes NLRP3-mediated β-cell Pyroptosis,” Cell Death Discovery 10, no. 1 (2024): 340.

[38]

T. Zhang, Y. Dong, Z. Li, et al., “STING-FSP1 Signaling Drives Endothelial Ferroptosis and Vascular Leakage in Sepsis,” International Immunopharmacology 168, no. Pt 2 (2026): 115892.

[39]

S. Ciardullo, M. Vergani, M. Rizzo, et al., “Qualitative Properties of Circulating Fatty Acids Are Associated With MASLD: A Cross-Sectional Study From the NHANES Database,” Liver Int Off J Int Assoc Study Liver 45, no. 12 (2025): e70441.

[40]

C. Cadagan, J. Russell-Guzmán, L. Américo-Da-Silva, et al., “Disulfiram Inhibits Gasdermin D Pores Formation and Improves Insulin-dependent Glucose Uptake and Glucose Homeostasis in Skeletal Muscle of Obesity-induced Insulin-resistant mice,” Scientific Reports (2025), Published online November 26.

[41]

D. C. Levine, R. H. Reeh, T. McMahon, T. Mandrup-Poulsen, Y. H. Fu, and L. J. Ptáček, “Unsaturated Fat Alters Clock Phosphorylation to Align Rhythms to the Season in Mice,” Science 390, no. 6771 (2025): eadp3065.

[42]

A. A. Spector and M. A. Yorek, “Membrane Lipid Composition and Cellular Function,” Journal of Lipid Research 26, no. 9 (1985): 1015–1035.

[43]

B. K. Tan, H. Xu, J. W. Sandberg, G. Brannigan, and W. W. L. Cheng, “Structural Mechanism of Lipid Modulation of Pentameric Ligand-gated Ion Channel Activity,” BioRxiv Prepr Serv Biol 2025 (2025), Published online October 7, 10.07.680764.

[44]

Y. Han, Z. Zhou, R. Jin, et al., “Mechanical Activation Opens a Lipid-lined Pore in OSCA Ion Channels,” Nature 628, no. 8009 (2024): 910–918.

[45]

E. E. Pohl, M. Vazdar, and J. Kreiter, “Exploring the Proton Transport Mechanism of the Mitochondrial ADP/ATP Carrier: FA-cycling Hypothesis and Beyond,” Protein Science: A Publication of The Protein Society 34, no. 3 (2025): e70047.

[46]

T. Chen, F. Vallese, E. Gil-Iturbe, et al., “Impact of Anionic Lipids on the Energy Landscape of Conformational Transition in Anion Exchanger 1 (AE1),” Nature Communications (2025), Published online November 26.

[47]

Y. Chen, J. Zhang, W. Cui, and R. L. Silverstein, “CD36, a Signaling Receptor and Fatty Acid Transporter That Regulates Immune Cell Metabolism and Fate,” Journal of Experimental Medicine 219, no. 6 (2022): e20211314.

[48]

J. F. C. Glatz and J. Luiken, “Dynamic Role of the Transmembrane Glycoprotein CD36 (SR-B2) in Cellular Fatty Acid Uptake and Utilization,” Journal of Lipid Research 59, no. 7 (2018): 1084–1093.

[49]

A. Bezawork-Geleta, C. J. Devereux, S. N. Keenan, et al., “Proximity Proteomics Reveals a Mechanism of Fatty Acid Transfer at Lipid Droplet-mitochondria- endoplasmic Reticulum Contact Sites,” Nature Communications 16, no. 1 (2025): 2135.

[50]

H. Qiu, C. Miao, and C. Ye, “An Adaptive Organelle Triad Houses Lipid Droplets for Dynamic Regulation,” Cell Reports 44, no. 6 (2025): 115813.

[51]

I. Álvarez-Guerra, E. Block, F. Broeskamp, et al., “LDO Proteins and Vac8 Form a Vacuole-lipid Droplet Contact Site to Enable Starvation-induced Lipophagy in Yeast,” Developmental Cell 59, no. 6 (2024): 759–775.e5.

[52]

S. Bolz, N. Kaempf, D. Puchkov, et al., “Synaptotagmin 1-triggered Lipid Signaling Facilitates Coupling of Exo- and Endocytosis,” Neuron 111, no. 23 (2023): 3765–3774.e7.

[53]

S. T. Glaser, K. Jayanetti, S. Oubraim, et al., “Fatty Acid Binding Proteins Are Novel Modulators of Synaptic Epoxyeicosatrienoic Acid Signaling in the Brain,” Scientific Reports 13, no. 1 (2023): 15234.

[54]

J. Hällqvist, C. E. Toomey, R. Pinto, et al., “Multi-omic Analysis Reveals Lipid Dysregulation Associated With Mitochondrial Dysfunction in parkinson's disease Brain,” Nature Communications 16, no. 1 (2025): 10490.

[55]

B. Kim, M. Yuk, M. Park, et al., “CRISPR Editing of miR-33 Restores ApoE Lipidation and Amyloid-β Metabolism in ApoE4 Sporadic Alzheimer's Disease,” Brain:A Journal of Neurology 148, no. 12 (2025): 4400–4415.

[56]

J. Cabot, A. J. Santillan, P. Férnandez-García, et al., “Fat for Thought: Lipid Regulation of Neural Stem Cell Fate,” Biomed Pharmacother Biomedecine Pharmacother 193 (2025): 118785.

[57]

D. Samovski, M. Jacome-Sosa, and N. A. Abumrad, “Fatty Acid Transport and Signaling: Mechanisms and Physiological Implications,” Annual Review of Physiology 85 (2023): 317–337.

[58]

R. Virk, K. Cook, A. Cavazos, S. R. Wassall, K. M. Gowdy, and S. R. Shaikh, “How Membrane Phospholipids Containing Long-Chain Polyunsaturated Fatty Acids and Their Oxidation Products Orchestrate Lipid Raft Dynamics to Control Inflammation,” Journal of Nutrition 154, no. 9 (2024): 2862–2870.

[59]

V. E. Kagan, Y. Y. Tyurina, I. I. Vlasova, et al., “Redox Epiphospholipidome in Programmed Cell Death Signaling: Catalytic Mechanisms and Regulation,” Front Endocrinol 11 (2020): 628079.

[60]

J. Xu, C. Fu, Y. Sun, et al., “Untargeted and Oxylipin-Targeted Metabolomics Study on the Plasma Samples of Primary Open-Angle Glaucoma Patients,” Biomolecules 14, no. 3 (2024): 307.

[61]

P. Malaiwong, A. F. Schroeder, T. Brown, et al., “Nuclear Receptor-neurotransmitter Coupling Links Behavior to Metabolic State,” BioRxiv Prepr Serv Biol 2025 (2025), Published online October 21, 10.20.683577.

[62]

H. Cai, X. Lin, L. Zhao, et al., “Noncanonical Agonist-dependent and -independent Arrestin Recruitment of GPR1,” Science 390, no. 6775 (2025): eadt8794.

[63]

L. M. T. Dicks, “Key Signals Produced by Gut Microbiota Associated With Metabolic Syndrome, Cancer, Cardiovascular Diseases, and Brain Functions,” International Journal of Molecular Sciences 26, no. 21 (2025): 10539.

[64]

F. Kemp, E. L. Braverman, and C. A. Byersdorfer, “Fatty Acid Oxidation in Immune Function,” Frontiers in immunology 15 (2024): 1420336.

[65]

M. Tian, F. Hao, X. Jin, et al., “KLHL25-ACLY Module Functions as a Switch in the Fate Determination of the Differentiation of iTreg/Th17,” Communications Biology 8, no. 1 (2025): 471.

[66]

J. Liang, J. Liao, R. Chang, et al., “Riplet Promotes Lipid Metabolism Changes Associated With CD8 T Cell Exhaustion and Anti-PD-1 Resistance in Hepatocellular Carcinoma,” Science Immunology 10, no. 108 (2025): eado3485.

[67]

S. Dalangood, C. Hu, C. Yuan, et al., “Cancer-associated Adipocytes Mediate CD8+T Cell Dysfunction via FGF21-driven Lipolysis,” Cell Reports 44, no. 11 (2025): 116526.

[68]

A. Douglas, B. Stevens, M. Rendas, et al., “Rhythmic IL-17 Production by Γδ T Cells Maintains Adipose De Novo Lipogenesis,” Nature 636, no. 8041 (2024): 206–214.

[69]

Y. Park, J. M. Woo, J. Shin, et al., “Unveiling the Biological Activities of the Microbial Long Chain Hydroxy Fatty Acids as Dual Agonists of GPR40 and GPR120,” Food Chemistry 465, no. Pt 1 (2025): 142010.

[70]

F. Li, L. Tai, X. Sun, et al., “Molecular Recognition and Activation Mechanism of Short-chain Fatty Acid Receptors FFAR2/3,” Cell Research 34, no. 4 (2024): 323–326.

[71]

Q. Zhang, Y. Wang, J. Zhu, et al., “Specialized Pro-resolving Lipid Mediators: A Key Player in Resolving Inflammation in Autoimmune Diseases,” Science Bulletin 70, no. 5 (2025): 778–794.

[72]

Y. Ding, Y. Wang, C. Li, et al., “Linolenic Acid Attenuates Pseudo-allergic Reactions by Inhibiting Lyn Kinase Activity,” Phytomedicine Int J Phytother Phytopharm 80 (2021): 153391.

[73]

C. Choi, Y. L. Jeong, K. M. Park, et al., “TM4SF19-mediated Control of Lysosomal Activity in Macrophages Contributes to Obesity-induced Inflammation and Metabolic Dysfunction,” Nature Communications 15, no. 1 (2024): 2779.

[74]

L. Tan, T. Lu, J. Lu, et al., “WTAP-m6A-ALOX15 Axis Mediates Dendritic Cells-keratinocytes Interaction Involved in Lipid Metabolism Disorders to Drive Atopic Dermatitis,” Life Sciences 385 (2026): 124110.

[75]

S. Alhmoudi, H. A. Kader, K. Alia, et al., “Pentanoate Modulates B Cells to Suppress Allergic Contact Hypersensitivity,” Scientific Reports 15, no. 1 (2025): 35803.

[76]

H. Guo, W. C. Liu, Y. Y. Sun, X. C. Jin, and P. P. Geng, “Neuroglia and Immune Cells Play Different Roles in Neuroinflammation and Neuroimmune Response in Post-stroke Neural Injury and Repair,” Acta Pharmacologica Sinica 47, no. 2 (2026): 273–289.

[77]

Y. Matsuzaka and M. Iyoda, “The IL-33/ST2/ILC2 Pathway in Kidney Disease: Balancing Inflammation, Fibrosis, and Repair,” American Journal of Physiology. Cell Physiology 329, no. 3 (2025): C718–C725.

[78]

Y. Yi, W. Xu, P. Mi, et al., “Deubiquitinase-dependent Transcriptional Silencing Controls Inflammation,” Cell Research 35, no. 9 (2025): 675–686.

[79]

H. Xiao, Y. Cao, P. Lizano, et al., “Interleukin-1β Moderates the Relationships Between Middle Frontal-mACC/Insular Connectivity and Depressive Symptoms in bipolar II Depression,” Brain, Behavior, and Immunity 120 (2024): 44–53.

[80]

J. Chen, C. Huang, T. Chen, et al., “Monocyte/Macrophage-derived NLRP3 Promotes the Onset and Progression of Ankylosing Spondylitis via the NOD-Like Receptor Pathway,” Journal of Clinical Immunology 45, no. 1 (2025): 169.

[81]

S. M. Hwang, D. Awasthi, J. Jeong, et al., “Transgelin 2 Guards T Cell Lipid Metabolism and Antitumour Function,” Nature 635, no. 8040 (2024): 1010–1018.

[82]

Y. Cui, Z. Feng, Q. Zhao, et al., “Immunocyte Lipid Metabolic Reprogramming: A Novel Pathway for Targeted Intervention in Autoimmune Diseases,” Frontiers in immunology 16 (2025): 1713148.

[83]

M. Lochner, L. Berod, and T. Sparwasser, “Fatty Acid Metabolism in the Regulation of T Cell Function,” Trends in Immunology 36, no. 2 (2015): 81–91.

[84]

Y. Chen and P. Li, “Fatty Acid Metabolism and Cancer Development,” Science Bulletin 61, no. 19 (2016): 1473–1479.

[85]

I. L. Rudolph, D. S. Kelley, K. C. Klasing, and K. L. Erickson, “Regulation of Cellular Differentiation and Apoptosis by Fatty Acids and Their Metabolites,” Nutrition Research 21, no. 1 (2001): 381–393.

[86]

C. Huang and C. Freter, “Lipid Metabolism, Apoptosis and Cancer Therapy,” International Journal of Molecular Sciences 16, no. 1 (2015): 924–949.

[87]

S. Dikalov, A. Panov, and A. Dikalova, “Critical Role of Mitochondrial Fatty Acid Metabolism in Normal Cell Function and Pathological Conditions,” International Journal of Molecular Sciences 25, no. 12 (2024): 6498.

[88]

A. Mantovani, P. Allavena, A. Sica, and F. Balkwill, “Cancer-related Inflammation,” Nature 454, no. 7203 (2008): 436–444.

[89]

J. Xu, B. Zheng, C. Xie, et al., “Inhibition of FABP5 Attenuates Inflammatory Bowel Disease by Modulating Macrophage Alternative Activation,” Biochemical Pharmacology 219 (2024): 115974.

[90]

L. Catrysse, B. Maes, P. Mehrotra, et al., “A20 deficiency in Myeloid Cells Protects Mice From Diet-induced Obesity and Insulin Resistance due to Increased Fatty Acid Metabolism,” Cell Reports 36, no. 12 (2021): 109748.

[91]

G. Zhang, L. Ma, L. Bai, et al., “Inflammatory Microenvironment-targeted Nanotherapies,” Journal of Controlled Release 334 (2021): 114–126.

[92]

A. R. Johnson, J. J. Milner, and L. Makowski, “The Inflammation Highway: Metabolism Accelerates Inflammatory Traffic in Obesity,” Immunological Reviews 249, no. 1 (2012): 218–238.

[93]

J. Hou, M. Karin, and B. Sun, “Targeting Cancer-promoting Inflammation—have Anti-inflammatory Therapies Come of Age?” Nature Reviews Clinical Oncology 18, no. 5 (2021): 261–279.

[94]

N. Koundouros and G. Poulogiannis, “Reprogramming of Fatty Acid Metabolism in Cancer,” British Journal of Cancer 122, no. 1 (2020): 4–22.

[95]

F. A. Kuehl and R. W. Egan, “Prostaglandins, Arachidonic Acid, and Inflammation,” Science 210, no. 4473 (1980): 978–984.

[96]

W. R. Henderson, “The Role of Leukotrienes in Inflammation,” Annals of Internal Medicine 121, no. 9 (1994): 684–697.

[97]

W. L. Smith, D. L. DeWitt, and R. M. Garavito, “Cyclooxygenases: Structural, Cellular, and Molecular Biology,” Annual Review of Biochemistry 69 (2000): 145–182.

[98]

O. Rådmark, O. Werz, D. Steinhilber, and B. Samuelsson, “5-Lipoxygenase: Regulation of Expression and Enzyme Activity,” Trends in Biochemical Sciences 32, no. 7 (2007): 332–341.

[99]

O. Rådmark and B. Samuelsson, “5-Lipoxygenase: Mechanisms of Regulation,” Journal of Lipid Research 50, no. Suppl (2009): S40–45.

[100]

M. O. Freire and T. E. Van Dyke, “Natural Resolution of Inflammation,” Periodontology 2000 63, no. 1 (2013): 149–164.

[101]

N. Chiang and C. N. Serhan, “Specialized Pro-resolving Mediator network: An Update on Production and Actions,” Essays in Biochemistry 64, no. 3 (2020): 443–462.

[102]

L. V. Norling and C. N. Serhan, “Profiling in Resolving Inflammatory Exudates Identifies Novel Anti-inflammatory and Pro-resolving Mediators and Signals for Termination,” Journal of Internal Medicine 268, no. 1 (2010): 15–24.

[103]

P. C. Calder, “Long-chain Fatty Acids and Inflammation,” Proceedings of the Nutrition Society 71, no. 2 (2012): 284–289.

[104]

C. N. Serhan and B. D. Levy, “Resolvins in Inflammation: Emergence of the Pro-resolving Superfamily of Mediators,” Journal of Clinical Investigation 128, no. 7 (2018): 2657–2669.

[105]

P. Singer, H. Shapiro, M. Theilla, R. Anbar, J. Singer, and J. Cohen, “Anti-inflammatory Properties of Omega-3 Fatty Acids in Critical Illness: Novel Mechanisms and an Integrative Perspective,” Intensive Care Medicine 34, no. 9 (2008): 1580–1592.

[106]

S. Krishnamoorthy, A. Recchiuti, N. Chiang, et al., “Resolvin D1 Binds human Phagocytes With Evidence for Proresolving Receptors,” PNAS 107, no. 4 (2010): 1660–1665.

[107]

S. Sánchez-García, R. I. Jaén, M. Fernández-Velasco, C. Delgado, L. Boscá, and P. Prieto, “Lipoxin-mediated Signaling: ALX/FPR2 Interaction and Beyond,” Pharmacological Research 197 (2023): 106982.

[108]

M. Arita, F. Bianchini, J. Aliberti, et al., “Stereochemical Assignment, Antiinflammatory Properties, and Receptor for the Omega-3 Lipid Mediator Resolvin E1,” Journal of Experimental Medicine 201, no. 5 (2005): 713–722.

[109]

N. Chiang, S. Libreros, P. C. Norris, X. de la Rosa, and C. N. Serhan, “Maresin 1 Activates LGR6 Receptor Promoting Phagocyte Immunoresolvent Functions,” Journal of Clinical Investigation 129, no. 12 (2019): 5294–5311.

[110]

S. Bang, Y. K. Xie, Z. J. Zhang, Z. Wang, Z. Z. Xu, and R. R. Ji, “GPR37 regulates Macrophage Phagocytosis and Resolution of Inflammatory Pain,” Journal of Clinical Investigation 128, no. 8 (2018): 3568–3582.

[111]

A. Rajendiran, S. H. Subramanyam, P. Klemm, et al., “NRF2/Itaconate Axis Regulates Metabolism and Inflammatory Properties of T Cells in Children With JIA,” Antioxidants 11, no. 12 (2022): 2426.

[112]

H. B. Ferreira, T. Melo, A. Paiva, M. Domingues, and R. do, “Insights in the Role of Lipids, Oxidative Stress and Inflammation in Rheumatoid Arthritis Unveiled by New Trends in Lipidomic Investigations,” Antioxidants Basel Switzerland 10, no. 1 (2021): 45.

[113]

D. S. Im, “Omega-3 Fatty Acids in Anti-inflammation (pro-resolution) and GPCRs,” Progress in Lipid Research 51, no. 3 (2012): 232–237.

[114]

S. Reuter, S. C. Gupta, M. M. Chaturvedi, and B. B. Aggarwal, “Oxidative Stress, Inflammation, and Cancer: How Are They Linked?” Free Radical Biology and Medicine 49, no. 11 (2010): 1603–1616.

[115]

L. B. Meira, J. M. Bugni, S. L. Green, et al., “DNA Damage Induced by Chronic Inflammation Contributes to Colon Carcinogenesis in Mice,” Journal of Clinical Investigation 118, no. 7 (2008): 2516–2525.

[116]

Y. Tanaka, L. M. Aleksunes, R. L. Yeager, et al., “NF-E2-related Factor 2 Inhibits Lipid Accumulation and Oxidative Stress in Mice Fed a High-fat Diet,” Journal of Pharmacology and Experimental Therapeutics 325, no. 2 (2008): 655–664.

[117]

H. Zhao, L. Wu, G. Yan, et al., “Inflammation and Tumor Progression: Signaling Pathways and Targeted Intervention,” Signal Transduct Target Ther 6, no. 1 (2021): 263.

[118]

V. Rogovskii, “Modulation of Inflammation-Induced Tolerance in Cancer,” Frontiers in Immunology 11 (2020): 1180.

[119]

L. Li, R. Yu, T. Cai, et al., “Effects of Immune Cells and Cytokines on Inflammation and Immunosuppression in the Tumor Microenvironment,” International Immunopharmacology 88 (2020): 106939.

[120]

S. Filiberti, M. Russo, S. Lonardi, et al., “Self-Renewal of Macrophages: Tumor-Released Factors and Signaling Pathways,” Biomedicines 10, no. 11 (2022): 2709.

[121]

X. Wu, T. Yang, X. Liu, et al., “IL-17 Promotes Tumor Angiogenesis Through Stat3 Pathway Mediated Upregulation of VEGF in Gastric Cancer,” Tumour Biology:journal of the International Society for Oncodevelopmental Biology and Medicine 37, no. 4 (2016): 5493–5501.

[122]

A. G. Jarnicki, J. Lysaght, S. Todryk, and K. H. G. Mills, “Suppression of Antitumor Immunity by IL-10 and TGF-beta-producing T Cells Infiltrating the Growing Tumor: Influence of Tumor Environment on the Induction of CD4+ and CD8+ Regulatory T Cells,” J Immunol 177, no. 2 (2006): 896–904.

[123]

D. Cruceriu, O. Baldasici, O. Balacescu, and I. Berindan-Neagoe, “The Dual Role of Tumor Necrosis Factor-alpha (TNF-α) in Breast Cancer: Molecular Insights and Therapeutic Approaches,” Cellular Oncology (Dordrecht, Netherlands) 43, no. 1 (2020): 1–18.

[124]

A. Mantovani, C. A. Dinarello, M. Molgora, and C. Garlanda, “Interleukin-1 and Related Cytokines in the Regulation of Inflammation and Immunity,” Immunity 50, no. 4 (2019): 778–795.

[125]

S. A. Jones and B. J. Jenkins, “Recent Insights Into Targeting the IL-6 Cytokine family in Inflammatory Diseases and Cancer,” Nature Reviews Immunology 18, no. 12 (2018): 773–789.

[126]

K. Fousek, L. A. Horn, and C. Palena, “Interleukin-8: A Chemokine at the Intersection of Cancer Plasticity, Angiogenesis, and Immune Suppression,” Pharmacology & Therapeutics 219 (2021): 107692.

[127]

M. Saraiva, P. Vieira, and A. O'Garra, “Biology and Therapeutic Potential of Interleukin-10,” Journal of Experimental Medicine 217, no. 1 (2020): e20190418.

[128]

E. D. Tait Wojno, C. A. Hunter, and J. S. Stumhofer, “The Immunobiology of the Interleukin-12 Family: Room for Discovery,” Immunity 50, no. 4 (2019): 851–870.

[129]

L. Wang, T. Yi, M. Kortylewski, D. M. Pardoll, D. Zeng, and H. Yu, “IL-17 Can Promote Tumor Growth Through an IL-6-Stat3 Signaling Pathway,” Journal of Experimental Medicine 206, no. 7 (2009): 1457–1464.

[130]

S. L. Gaffen, R. Jain, A. V. Garg, and D. J. Cua, “The IL-23-IL-17 Immune Axis: From Mechanisms to Therapeutic Testing,” Nature Reviews Immunology 14, no. 9 (2014): 585–600.

[131]

J. L. Langowski, X. Zhang, L. Wu, et al., “IL-23 Promotes Tumour Incidence and Growth,” Nature 442, no. 7101 (2006): 461–465.

[132]

M. W. L. Teng, D. M. Andrews, N. McLaughlin, et al., “IL-23 Suppresses Innate Immune Response Independently of IL-17A During Carcinogenesis and Metastasis,” PNAS 107, no. 18 (2010): 8328–8333.

[133]

S. Colak and P. Ten Dijke, “Targeting TGF-β Signaling in Cancer,” Trends in cancer 3, no. 1 (2017): 56–71.

[134]

E. Batlle and J. Massagué, “Transforming Growth Factor-β Signaling in Immunity and Cancer,” Immunity 50, no. 4 (2019): 924–940.

[135]

H. F. Dvorak, “Vascular Permeability Factor/Vascular Endothelial Growth Factor: A Critical Cytokine in Tumor Angiogenesis and a Potential Target for Diagnosis and Therapy,” Journal of Clinical Oncology: Official Journal of the American Society of Clinical Oncology 20, no. 21 (2002): 4368–4380.

[136]

P. Carmeliet and R. K. Jain, “Molecular Mechanisms and Clinical Applications of Angiogenesis,” Nature 473, no. 7347 (2011): 298–307.

[137]

D. Fukumura, J. Kloepper, Z. Amoozgar, D. G. Duda, and R. K. Jain, “Enhancing Cancer Immunotherapy Using Antiangiogenics: Opportunities and Challenges,” Nature Reviews Clinical Oncology 15, no. 5 (2018): 325–340.

[138]

K. Lei, J. Chen, Y. Deng, et al., “Cracking the Code of Cancer Immunotherapy Resistance: Emerging Roles of Pyroptosis and Necroptosis,” Journal of Experimental & Clinical Cancer Research 44, no. 1 (2025): 308.

[139]

GBD 2023 Cancer Collaborators. The Global, Regional, and National Burden of Cancer, 1990-2023, with forecasts to 2050: A systematic analysis for the Global Burden of Disease Study 2023. The Lancet (London, England) 2025; 406(10512): 1565–1586.

[140]

F. Bray, M. Laversanne, H. Sung, et al., “Global Cancer Statistics 2022: GLOBOCAN Estimates of Incidence and Mortality Worldwide for 36 Cancers in 185 Countries,” CA: A Cancer Journal for Clinicians 74, no. 3 (2024): 229–263.

[141]

S. K. Rehman, J. Haynes, E. Collignon, et al., “Colorectal Cancer Cells Enter a Diapause-Like DTP State to Survive Chemotherapy,” Cell 184, no. 1 (2021): 226–242.e21.

[142]

M. K. Callaway, B. J. Noonan, K. L. Schwertfeger, and P. P. Provenzano, “Extracellular Matrix Architecture Promotes Immunosuppressive Microenvironments in Pancreatic Cancer,” Matrix Biology: Journal of the International Society for Matrix Biology 141 (2025): 114–126.

[143]

S. Cassim and J. Pouyssegur, “Tumor Microenvironment: A Metabolic Player That Shapes the Immune Response,” International Journal of Molecular Sciences 21, no. 1 (2019): 157.

[144]

S. Yuan, J. Almagro, and E. Fuchs, “Beyond Genetics: Driving Cancer With the Tumour Microenvironment Behind the Wheel,” Nature Reviews Cancer 24, no. 4 (2024): 274–286.

[145]

Y. Fei, X. Cao, and J. Liu, “Nutritional Competition Within Tumor Microenvironment Dictates Anti-tumor Immunity,” National Science Review 11, no. 2 (2024): nwad277.

[146]

R. F. Tian, L. L. Feng, X. Liang, et al., “Carnitine Palmitoyltransferase 2 as a Novel Prognostic Biomarker and Immunoregulator in Colorectal Cancer,” International Journal of Biological Macromolecules 309, no. Pt 3 (2025): 142945.

[147]

E. G. Hunt, K. E. Hurst, B. P. Riesenberg, et al., “Acetyl-CoA Carboxylase Obstructs CD8+ T Cell Lipid Utilization in the Tumor Microenvironment,” Cell Metabolism 36, no. 5 (2024): 969–983.e10.

[148]

Y. Ping, Q. Fan, and Y. Zhang, “Modulating Lipid Metabolism Improves Tumor Immunotherapy,” Journal for ImmunoTherapy of Cancer 13, no. 2 (2025): e010824.

[149]

Q. Zhan, H. Ni, M. Zhou, et al., “Recent Advances in Understanding the Relationship Between Lipid Metabolism and Immune Escape in the Tumor Microenvironment of Gastric Cancer,” Medical Review 2021 5, no. 5 (2025): 378–399.

[150]

L. Zhang, J. Zhao, C. Su, et al., “Organoid Models of Ovarian Cancer: Resolving Immune Mechanisms of Metabolic Reprogramming and Drug Resistance,” Frontiers in Immunology 16 (2025): 1573686.

[151]

N. Aoki, G. Wakisaka, and I. Nagata, “Increase of T Cells in Graves' disease,” The Lancet (London, England) 2, no. 7819 (1973): 49–50.

[152]

M. Zhai, Z. Zhang, J. Dong, et al., “Spatial Proteomic Profiling Reveals Conserved Prognostic Immune Microenvironment Features Across Molecular Subtypes in Small Cell Lung Cancer,” Pharmacological Research 222 (2025): 108048.

[153]

M. Sang, J. Ge, J. Ge, et al., “Immune Regulatory Genes Impact the Hot/Cold Tumor Microenvironment, Affecting Cancer Treatment and Patient Outcomes,” Frontiers in Immunology 15 (2024): 1382842.

[154]

O. Ali and A. Szabó, “Review of Eukaryote Cellular Membrane Lipid Composition, with Special Attention to the Fatty Acids,” International Journal of Molecular Sciences 24, no. 21 (2023): 15693.

[155]

G. van Meer, D. R. Voelker, and G. W. Feigenson, “Membrane Lipids: Where They Are and How They Behave,” Nature Reviews Molecular Cell Biology 9, no. 2 (2008): 112–124.

[156]

D. Mondal, R. Dutta, P. Banerjee, D. Mukherjee, T. K. Maiti, and N. Sarkar, “Modulation of Membrane Fluidity Performed on Model Phospholipid Membrane and Live Cell Membrane: Revealing Through Spatiotemporal Approaches of FLIM, FAIM, and TRFS,” Analytical Chemistry 91, no. 7 (2019): 4337–4345.

[157]

C. Corbet, E. Bastien, J. P. Santiago de Jesus, et al., “TGFβ2-induced Formation of Lipid Droplets Supports Acidosis-driven EMT and the Metastatic Spreading of Cancer Cells,” Nature Communications 11, no. 1 (2020): 454.

[158]

Z. H. Wen, Y. C. Su, P. L. Lai, et al., “Critical Role of Arachidonic Acid-activated mTOR Signaling in Breast Carcinogenesis and Angiogenesis,” Oncogene 32, no. 2 (2013): 160–170.

[159]

D. Wang and R. N. Dubois, “Eicosanoids and Cancer,” Nature Reviews Cancer 10, no. 3 (2010): 181–193.

[160]

G. O'Callaghan and A. Houston, “Prostaglandin E2 and the EP Receptors in Malignancy: Possible Therapeutic Targets?” British Journal of Pharmacology 172, no. 22 (2015): 5239–5250.

[161]

A. Filippelli, V. Ciccone, C. Del Gaudio, et al., “ERK5 mediates Pro-tumorigenic Phenotype in Non-small Lung Cancer Cells Induced by PGE2,” Biochimica et Biophysica Acta (BBA) - Molecular Cell Research 1871, no. 7 (2024): 119810.

[162]

S. Zhang, K. Lv, Z. Liu, R. Zhao, and F. Li, “Fatty Acid Metabolism of Immune Cells: A New Target of Tumour Immunotherapy,” Cell Death Discovery 10, no. 1 (2024): 1–12.

[163]

Q. Li, R. Zhao, Y. Shen, et al., “Lactylation in Tumor Immune Escape and Immunotherapy: Multifaceted Functions and Therapeutic Strategies,” Res Wash DC 8 (2025): 0793.

[164]

N. H. Son, D. Basu, D. Samovski, et al., “Endothelial Cell CD36 Optimizes Tissue Fatty Acid Uptake,” Journal of Clinical Investigation 128, no. 10 (2018): 4329–4342.

[165]

J. Wang and Y. Li, “CD36 tango in Cancer: Signaling Pathways and Functions,” Theranostics 9, no. 17 (2019): 4893–4908.

[166]

H. Wang, F. Franco, Y. C. Tsui, et al., “CD36-mediated Metabolic Adaptation Supports Regulatory T Cell Survival and Function in Tumors,” Nature Immunology 21, no. 3 (2020): 298–308.

[167]

X. Ma, L. Xiao, L. Liu, et al., “CD36-mediated Ferroptosis Dampens Intratumoral CD8+ T Cell Effector Function and Impairs Their Antitumor Ability,” Cell Metabolism 33, no. 5 (2021): 1001–1012.

[168]

Y. Xiao, Y. Yang, H. Xiong, and G. Dong, “The Implications of FASN in Immune Cell Biology and Related Diseases,” Cell death & disease 15, no. 1 (2024): 1–12.

[169]

D. Vanauberg, C. Schulz, and T. Lefebvre, “Involvement of the Pro-oncogenic Enzyme Fatty Acid Synthase in the Hallmarks of Cancer: A Promising Target in Anti-cancer Therapies,” Oncogenesis 12, no. 1 (2023): 16.

[170]

S. A. Lim, J. Wei, T. L. M. Nguyen, et al., “Lipid Signalling Enforces Functional Specialization of Treg Cells in Tumours,” Nature 591, no. 7849 (2021): 306–311.

[171]

E. Cuyàs, S. Pedarra, S. Verdura, et al., “Fatty Acid Synthase (FASN) Is a Tumor-cell-intrinsic Metabolic Checkpoint Restricting T-cell Immunity,” Cell Death Discovery 10 (2024): 417.

[172]

Y. Endo, A. Onodera, K. Obata-Ninomiya, et al., “ACC1 determines Memory Potential of Individual CD4+ T Cells by Regulating De Novo Fatty Acid Biosynthesis,” Nature Metabolism 1, no. 2 (2019): 261–275.

[173]

T. Nakajima, T. Kanno, Y. Ueda, et al., “Fatty Acid Metabolism Constrains Th9 Cell Differentiation and Antitumor Immunity via the Modulation of Retinoic Acid Receptor Signaling,” Cellular & Molecular Immunology (2024), Published online August 26.

[174]

L. Hodson and B. A. Fielding, “Stearoyl-CoA Desaturase: Rogue or Innocent Bystander?” Progress in Lipid Research 52, no. 1 (2013): 15–42.

[175]

Y. Bai, J. G. McCoy, E. J. Levin, et al., “X-ray Structure of a Mammalian Stearoyl-CoA Desaturase,” Nature 524, no. 7564 (2015): 252–256.

[176]

Y. Katoh, T. Yaguchi, A. Kubo, et al., “Inhibition of Stearoyl-CoA Desaturase 1 (SCD1) Enhances the Antitumor T Cell Response Through Regulating β-catenin Signaling in Cancer Cells and ER Stress in T Cells and Synergizes With Anti-PD-1 Antibody,” Journal for ImmunoTherapy of Cancer 10, no. 7 (2022): e004616.

[177]

T. Sugi, Y. Katoh, T. Ikeda, et al., “SCD1 inhibition Enhances the Effector Functions of CD8+ T Cells via ACAT1-dependent Reduction of Esterified Cholesterol,” Cancer Science 115, no. 1 (2024): 48–58.

[178]

J. Qin, L. Ye, X. Wen, et al., “Fatty Acids in Cancer Chemoresistance,” Cancer Letters 572 (2023): 216352.

[179]

Y. Tan, J. Li, G. Zhao, et al., “Metabolic Reprogramming From Glycolysis to Fatty Acid Uptake and Beta-oxidation in Platinum-resistant Cancer Cells,” Nature Communications 13, no. 1 (2022): 4554.

[180]

L. Zhang, Y. Sun, Y. Lin, et al., “Cell Calcification Reverses the Chemoresistance of Cancer Cells via the Conversion of Glycolipid Metabolism,” Biomaterials 314 (2025): 122886.

[181]

S. Luo, H. Yang, X. Jiang, et al., “Inhibition of Tumor Lipogenesis and Growth by Peptide-Based Targeting of SREBP Activation,” Adv Sci Weinh Baden-Wurtt Ger 12, no. 45 (2025): e08111.

[182]

Z. Han, Z. Yan, Z. Ma, et al., “Targeting ABCD1-ACOX1-MET/IGF1R Axis Suppresses Multiple Myeloma,” Leukemia 39, no. 3 (2025): 720–733.

[183]

M. Russo, M. Chen, E. Mariella, et al., “Cancer Drug-tolerant Persister Cells: From Biological Questions to Clinical Opportunities,” Nature Reviews Cancer 24, no. 10 (2024): 694–717.

[184]

J. He, Z. Qiu, J. Fan, X. Xie, Q. Sheng, and X. Sui, “Drug Tolerant Persister Cell Plasticity in Cancer: A Revolutionary Strategy for More Effective Anticancer Therapies,” Signal Transduct Target Ther 9, no. 1 (2024): 209.

[185]

S. Shen, S. Faouzi, S. Souquere, et al., “Melanoma Persister Cells Are Tolerant to BRAF/MEK Inhibitors via ACOX1-Mediated Fatty Acid Oxidation,” Cell reports 33, no. 8 (2020): 108421.

[186]

J. J. Loh and S. Ma, “Hallmarks of Cancer Stemness,” Cell Stem Cell 31, no. 5 (2024): 617–639.

[187]

M. Yi, J. Li, S. Chen, et al., “Emerging Role of Lipid Metabolism Alterations in Cancer Stem Cells,” Journal of Experimental & Clinical Cancer Research 37, no. 1 (2018): 118.

[188]

R. Paul, J. F. Dorsey, and Y. Fan, “Cell Plasticity, Senescence, and Quiescence in Cancer Stem Cells: Biological and Therapeutic Implications,” Pharmacology & Therapeutics 231 (2022): 107985.

[189]

T. Wang, J. F. Fahrmann, H. Lee, et al., “JAK/STAT3-Regulated Fatty Acid β-Oxidation Is Critical for Breast Cancer Stem Cell Self-Renewal and Chemoresistance,” Cell metabolism 27, no. 1 (2018): 136–150.e5.

[190]

M. Mascaraque, S. Courtois, A. Royo-García, et al., “Fatty Acid Oxidation Is Critical for the Tumorigenic Potential and Chemoresistance of Pancreatic Cancer Stem Cells,” Journal of Translational Medicine 22, no. 1 (2024): 797.

[191]

W. He, B. Liang, C. Wang, et al., “MSC-regulated lncRNA MACC1-AS1 Promotes Stemness and Chemoresistance Through Fatty Acid Oxidation in Gastric Cancer,” Oncogene 38, no. 23 (2019): 4637–4654.

[192]

H. Wu, B. Liu, Z. Chen, G. Li, and Z. Zhang, “MSC-induced lncRNA HCP5 Drove Fatty Acid Oxidation Through miR-3619-5p/AMPK/PGC1α/CEBPB Axis to Promote Stemness and Chemo-resistance of Gastric Cancer,” Cell death & disease 11, no. 4 (2020): 233.

[193]

X. Zhang, J. Wang, X. Li, and D. Wang, “Lysosomes Contribute to Radioresistance in Cancer,” Cancer Letters 439 (2018): 39–46.

[194]

Y. Yu, J. Yu, S. Ge, Y. Su, and X. Fan, “Novel Insight Into Metabolic Reprogrammming in Cancer Radioresistance: A Promising Therapeutic Target in Radiotherapy,” Int J Biol Sci 19, no. 3 (2023): 811–828.

[195]

L. Tang, F. Wei, Y. Wu, et al., “Role of Metabolism in Cancer Cell Radioresistance and Radiosensitization Methods,” Journal of Experimental & Clinical Cancer Research 37, no. 1 (2018): 87.

[196]

A. Mittal, M. Nenwani, I. Sarangi, A. Achreja, T. S. Lawrence, and D. Nagrath, “Radiotherapy-induced Metabolic Hallmarks in the Tumor Microenvironment,” Trends in Cancer 8, no. 10 (2022): 855–869.

[197]

Y. Cao, J. Li, Y. Chen, et al., “Monounsaturated Fatty Acids Promote Cancer Radioresistance by Inhibiting Ferroptosis Through ACSL3,” Cell Death & Disease 16, no. 1 (2025): 184.

[198]

Z. Tan, L. Xiao, M. Tang, et al., “Targeting CPT1A-mediated Fatty Acid Oxidation Sensitizes Nasopharyngeal Carcinoma to Radiation Therapy,” Theranostics 8, no. 9 (2018): 2329–2347.

[199]

Q. Du, Z. Tan, F. Shi, et al., “PGC1α/CEBPB/CPT1A Axis Promotes Radiation Resistance of Nasopharyngeal Carcinoma Through Activating Fatty Acid Oxidation,” Cancer Science 110, no. 6 (2019): 2050–2062.

[200]

N. Jiang, B. Xie, W. Xiao, et al., “Fatty Acid Oxidation Fuels Glioblastoma Radioresistance With CD47-mediated Immune Evasion,” Nature Communications 13, no. 1 (2022): 1511.

[201]

J. Liang, L. Liao, L. Xie, et al., “PITPNC1 Suppress CD8+ T Cell Immune Function and Promote Radioresistance in Rectal Cancer by Modulating FASN/CD155,” Journal of Translational Medicine 22, no. 1 (2024): 117.

[202]

C. I. Chen, D. Y. Kuo, and H. Y. Chuang, “FASN Inhibition Shows the Potential for Enhancing Radiotherapy Outcomes by Targeting Glycolysis, AKT, and ERK Pathways in Breast Cancer,” International Journal of Radiation Biology 101, no. 3 (2025): 292–303.

[203]

H. J. Burstein, C. Lacchetti, H. Anderson, et al., “Adjuvant Endocrine Therapy for Women with Hormone Receptor-Positive Breast Cancer: ASCO Clinical Practice Guideline Focused Update,” Journal of Clinical Oncology:Official Journal of the American Society of Clinical Oncology 37, no. 5 (2019): 423–438.

[204]

I. D. Davis, A. J. Martin, M. R. Stockler, et al., “Enzalutamide With Standard First-Line Therapy in Metastatic Prostate Cancer,” New England Journal of Medicine 381, no. 2 (2019): 121–131.

[205]

J. A. Menendez, A. Papadimitropoulou, T. Vander Steen, et al., “Fatty Acid Synthase Confers Tamoxifen Resistance to ER+/HER2+ Breast Cancer,” Cancers 13, no. 5 (2021): 1132.

[206]

L. Duan, S. Calhoun, D. Shim, R. E. Perez, L. A. Blatter, and C. G. Maki, “Fatty Acid Oxidation and Autophagy Promote Endoxifen Resistance and Counter the Effect of AKT Inhibition in ER-positive Breast Cancer Cells,” Journal of Molecular Cell Biology 13, no. 6 (2021): 433–444.

[207]

C. Jiang, Y. Zhu, H. Chen, et al., “Targeting c-Jun Inhibits Fatty Acid Oxidation to Overcome Tamoxifen Resistance in Estrogen Receptor-positive Breast Cancer,” Cell death & disease 14, no. 10 (2023): 653.

[208]

J. Yu, Y. Du, C. Liu, et al., “Low GPR81 in ER+ Breast Cancer Cells Drives Tamoxifen Resistance Through Inducing PPARα-mediated Fatty Acid Oxidation,” Life Sciences 350 (2024): 122763.

[209]

T. Karantanos, C. P. Evans, B. Tombal, T. C. Thompson, R. Montironi, and W. B. Isaacs, “Understanding the Mechanisms of Androgen Deprivation Resistance in Prostate Cancer at the Molecular Level,” European Urology 67, no. 3 (2015): 470–479.

[210]

C. F. Ribeiro, S. Rodrigues, D. C. Bastos, et al., “Blocking Lipid Synthesis Induces DNA Damage in Prostate Cancer and Increases Cell Death Caused by PARP Inhibition,” Science Signaling 17, no. 831 (2024): eadh1922.

[211]

W. Han, S. Gao, D. Barrett, et al., “Reactivation of Androgen Receptor-regulated Lipid Biosynthesis Drives the Progression of Castration-resistant Prostate Cancer,” Oncogene 37, no. 6 (2018): 710–721.

[212]

G. E. Stoykova and I. R. Schlaepfer, “Lipid Metabolism and Endocrine Resistance in Prostate Cancer, and New Opportunities for Therapy,” International Journal of Molecular Sciences 20, no. 11 (2019): 2626.

[213]

R. K. Shrestha, Z. D. Nassar, A. R. Hanson, et al., “ACSM1 and ACSM3 Regulate Fatty Acid Metabolism to Support Prostate Cancer Growth and Constrain Ferroptosis,” Cancer Research 84, no. 14 (2024): 2313–2332.

[214]

I. R. Schlaepfer, L. Rider, L. U. Rodrigues, et al., “Lipid Catabolism via CPT1 as a Therapeutic Target for Prostate Cancer,” Molecular Cancer Therapeutics 13, no. 10 (2014): 2361–2371.

[215]

G. Zadra, C. Photopoulos, S. Tyekucheva, et al., “A Novel Direct Activator of AMPK Inhibits Prostate Cancer Growth by Blocking Lipogenesis,” EMBO Molecular Medicine 6, no. 4 (2014): 519–538.

[216]

G. Zadra, C. F. Ribeiro, P. Chetta, et al., “Inhibition of De Novo Lipogenesis Targets Androgen Receptor Signaling in Castration-resistant Prostate Cancer,” PNAS 116, no. 2 (2019): 631–640.

[217]

J. Luo, Y. Hong, Y. Lu, et al., “Acetyl-CoA Carboxylase Rewires Cancer Metabolism to Allow Cancer Cells to Survive Inhibition of the Warburg Effect by cetuximab,” Cancer Letters 384 (2017): 39–49.

[218]

Y. J. Li, J. F. Fahrmann, M. Aftabizadeh, et al., “Fatty Acid Oxidation Protects Cancer Cells From Apoptosis by Increasing Mitochondrial Membrane Lipids,” Cell reports 39, no. 9 (2022): 110870.

[219]

A. Ali, E. Levantini, J. T. Teo, et al., “Fatty Acid Synthase Mediates EGFR Palmitoylation in EGFR Mutated Non-small Cell Lung Cancer,” EMBO Molecular Medicine 10, no. 3 (2018): e8313.

[220]

A. Talebi, V. De Laat, X. Spotbeen, et al., “Pharmacological Induction of Membrane Lipid Poly-unsaturation Sensitizes Melanoma to ROS Inducers and Overcomes Acquired Resistance to Targeted Therapy,” Journal of Experimental & Clinical Cancer Research 42, no. 1 (2023): 92.

[221]

M. Redondo-Muñoz, F. J. Rodriguez-Baena, P. Aldaz, et al., “Metabolic Rewiring Induced by ranolazine Improves Melanoma Responses to Targeted Therapy and Immunotherapy,” Nat Metab 5, no. 9 (2023): 1544–1562.

[222]

Q. Jin, L. X. Yuan, D. Boulbes, et al., “Fatty Acid Synthase Phosphorylation: A Novel Therapeutic Target in HER2-overexpressing Breast Cancer Cells,” Breast Cancer Research 12, no. 6 (2010): R96.

[223]

L. Castagnoli, S. Corso, A. Franceschini, et al., “Fatty Acid Synthase as a New Therapeutic Target for HER2-positive Gastric Cancer,” Cell Oncol Dordr Neth 46, no. 3 (2023): 661–676.

[224]

I. Nandi, L. Ji, H. W. Smith, et al., “Targeting Fatty Acid Oxidation Enhances Response to HER2-targeted Therapy,” Nature Communications 15, no. 1 (2024): 6587.

[225]

Z. Yang, L. Yang, Y. Wang, et al., “A Bibliometric Visualization of Resistance to Lung Cancer Immunotherapy: A Decade of Research Progress (2014-2024),” Frontiers in oncology 15 (2025): 1656967.

[226]

J. L. Hor, E. C. Schrom, A. Wong-Rolle, et al., “Inhibitory PD-1 Axis Maintains High-avidity Stem-Like CD8+ T Cells,” Nature 649, no. 8095 (2026): 194–204.

[227]

G. Guzelsoy, S. D. Elorza, M. Ros, et al., “Cooperative Nutrient Scavenging Is an Evolutionary Advantage in Cancer,” Nature 640, no. 8058 (2025): 534–542.

[228]

J. Jin, P. Yan, D. Wang, et al., “Targeting Lactylation Reinforces NK Cell Cytotoxicity Within the Tumor Microenvironment,” Nature Immunology 26, no. 7 (2025): 1099–1112.

[229]

Y. Gan, D. Meng, L. Lang, et al., “PLA2G16-Mediated Tetracosatetraenoic Acid Rewires Fatty Acid Oxidation to Impair CD8+ T Cell Immune Function in Promoting Breast Cancer Lung Metastasis,” Adv Sci (Weinh) 13, no. 6 (2026): e10224.

[230]

Y. Zeng, L. Zhao, K. Zeng, et al., “TRAF3 loss Protects Glioblastoma Cells From Lipid Peroxidation and Immune Elimination via Dysregulated Lipid Metabolism,” Journal of Clinical Investigation 135, no. 7 (2025): e178550.

[231]

J. Wen, X. Zhang, C. C. Wong, et al., “Targeting Squalene Epoxidase Restores Anti-PD-1 Efficacy in Metabolic Dysfunction-associated Steatohepatitis-induced Hepatocellular Carcinoma,” Gut 73, no. 12 (2024): 2023–2036.

[232]

L. Yu, K. Liebenberg, Y. Shen, et al., “Tumor-derived Arachidonic Acid Reprograms Neutrophils to Promote Immune Suppression and Therapy Resistance in Triple-negative Breast Cancer,” Immunity 58, no. 4 (2025): 909–925.e7.

[233]

Y. Li, Z. Chen, D. Wang, et al., “Transforming Acidic Coiled-coil-containing Protein 3-mediated Lipid Metabolism Reprogramming Impairs CD8+ T-cell Cytotoxicity in Hepatocellular Carcinoma,” Signal Transduct Target Ther 10, no. 1 (2025): 274.

[234]

N. Berrell, H. Sadeghirad, T. Blick, et al., “Metabolomics at the Tumor Microenvironment Interface: Decoding Cellular Conversations,” Medicinal Research Reviews 44, no. 3 (2024): 1121–1146.

[235]

C. Tay, A. Tanaka, and S. Sakaguchi, “Tumor-infiltrating Regulatory T Cells as Targets of Cancer Immunotherapy,” Cancer Cell 41, no. 3 (2023): 450–465.

[236]

M. J. Watson, P. D. A. Vignali, S. J. Mullett, et al., “Metabolic Support of Tumour-infiltrating Regulatory T Cells by Lactic Acid,” Nature 591, no. 7851 (2021): 645–651.

[237]

S. F. Tzeng, Y. R. Yu, J. Park, et al., “PLT012, a Humanized CD36-Blocking Antibody, Is Effective for Unleashing Antitumor Immunity against Liver Cancer and Liver Metastasis,” Cancer discovery 15, no. 8 (2025): 1676–1696.

[238]

J. J. Chen, M. Y. Vincent, D. Shepard, et al., “Phase 1 Dose Expansion and Biomarker Study Assessing First-in-class Tumor Microenvironment Modulator VT1021 in Patients With Advanced Solid Tumors,” Commun Med 4, no. 1 (2024): 95.

[239]

C. S. Field, F. Baixauli, R. L. Kyle, et al., “Mitochondrial Integrity Regulated by Lipid Metabolism Is a Cell-Intrinsic Checkpoint for Treg Suppressive Function,” Cell metabolism 31, no. 2 (2020): 422–437.e5.

[240]

S. Kobayashi, T. Wannakul, K. Sekino, et al., “Fatty Acid-binding Protein 5 Limits the Generation of Foxp3+ Regulatory T Cells Through Regulating Plasmacytoid Dendritic Cell Function in the Tumor Microenvironment,” International Journal of Cancer 150, no. 1 (2022): 152–163.

[241]

A. Christofides, L. Strauss, A. Yeo, C. Cao, A. Charest, and V. A. Boussiotis, “The Complex Role of Tumor-infiltrating Macrophages,” Nature Immunology 23, no. 8 (2022): 1148–1156.

[242]

L. Huang, F. Wang, X. Wang, et al., “M2-Like Macrophage-derived Exosomes Facilitate Metastasis in Non-small-cell Lung Cancer by Delivering Integrin αVβ3,” MedComm 4, no. 1 (2023): e191.

[243]

Y. Qian, Y. Yin, X. Zheng, Z. Liu, and X. Wang, “Metabolic Regulation of Tumor-associated Macrophage Heterogeneity: Insights Into the Tumor Microenvironment and Immunotherapeutic Opportunities,” Biomarker Research 12, no. 1 (2024): 1.

[244]

X. Yang, B. Deng, W. Zhao, et al., “FABP5+ lipid-loaded Macrophages Process Tumour-derived Unsaturated Fatty Acid Signal to Suppress T-cell Antitumour Immunity,” Journal of Hepatology 82, no. 4 (2025): 676–689.

[245]

B. F. Tang, W. T. Xu, S. J. Fang, et al., “MELK Prevents Radiofrequency Ablation-induced Immunogenic Cell Death and Antitumor Immune Response by Stabilizing FABP5 in Hepatocellular Malignancies,” Mil Med Res 12, no. 1 (2025): 5.

[246]

R. E. Dadey, R. Li, J. Griner, et al., “Multiomics Identifies Tumor-intrinsic SREBP1 Driving Immune Exclusion in Hepatocellular Carcinoma,” Journal for ImmunoTherapy of Cancer 13, no. 6 (2025): e011537.

[247]

J. Chang, Y. Niu, S. Zhou, et al., “DPP7 promotes Fatty Acid β-oxidation in Tumor-associated Macrophages and Determines Immunosuppressive Microenvironment in Colorectal Cancer,” Int J Biol Sci 21, no. 14 (2025): 6305–6325.

[248]

P. Yang, H. Qin, Y. Li, et al., “CD36-mediated Metabolic Crosstalk Between Tumor Cells and Macrophages Affects Liver Metastasis,” Nature Communications 13, no. 1 (2022): 5782.

[249]

S. M. Poznanski, K. Singh, T. M. Ritchie, et al., “Metabolic Flexibility Determines human NK Cell Functional Fate in the Tumor Microenvironment,” Cell metabolism 33, no. 6 (2021): 1205–1220.e5.

[250]

J. Yan, C. Zhang, Y. Xu, et al., “GPR34 is a Metabolic Immune Checkpoint for ILC1-mediated Antitumor Immunity,” Nature Immunology 25, no. 11 (2024): 2057–2067.

[251]

D. Jiao, R. Sun, X. Ren, et al., “Lipid Accumulation-mediated Histone Hypoacetylation Drives Persistent NK Cell Dysfunction in Anti-tumor Immunity,” Cell reports 42, no. 10 (2023): 113211.

[252]

NCD Risk Factor Collaboration (NCD-RisC). Worldwide Trends in Diabetes Prevalence and Treatment From 1990 to 2022: A Pooled Analysis of 1108 Population-representative Studies With 141 Million Participants. Lancet Lond Engl 2024; 404(10467): 2077–2093.

[253]

Z. Liu, X. Li, L. Liang, W. Cheng, and L. Zhao, “National and Regional Burden of Early-onset Type 2 Diabetes Mellitus in the Americas From 1990 to 2023, Attributable to Modifiable Risk Factors, and Projections to 2050: A Systematic Analysis for the Global Burden of Disease Study 2023,” Diabetes Research and Clinical Practice 231 (2025): 113007.

[254]

M. Roden, T. B. Price, G. Perseghin, et al., “Mechanism of Free Fatty Acid-induced Insulin Resistance in Humans,” J Clin Invest 97, no. 12 (1996): 2859–2865.

[255]

I. R. Jung, R. S. Ahima, and S. F. Kim, “Inositol Polyphosphate Multikinase Modulates Free Fatty Acids-induced Insulin Resistance in Primary Mouse Hepatocytes,” Journal of Cellular Biochemistry 124, no. 11 (2023): 1695–1704.

[256]

G. Perseghin, S. Ghosh, K. Gerow, and G. I. Shulman, “Metabolic Defects in Lean Nondiabetic Offspring of NIDDM Parents: A Cross-sectional Study,” Diabetes 46, no. 6 (1997): 1001–1009.

[257]

X. Deng, Y. Luo, Y. Gao, and T. Wu, “Long-chain Acyl-CoA Synthetases: Biological Functions, Diseases and Therapeutic Targets,” Mol Biomed 6, no. 1 (2025): 117.

[258]

X. Wang, Q. Wu, M. Zhong, et al., “Adipocyte-derived Ferroptotic Signaling Mitigates Obesity,” Cell metabolism 37, no. 3 (2025): 673–691.e7.

[259]

J. E. Kanter, C. Tang, J. F. Oram, and K. E. Bornfeldt, “Acyl-CoA Synthetase 1 Is Required for Oleate and Linoleate Mediated Inhibition of Cholesterol Efflux Through ATP-binding Cassette Transporter A1 in Macrophages,” Biochimica Et Biophysica Acta 1821, no. 3 (2012): 358–364.

[260]

P. A. Young, C. E. Senkal, A. L. Suchanek, et al., “Long-chain Acyl-CoA Synthetase 1 Interacts With Key Proteins That Activate and Direct Fatty Acids Into Niche Hepatic Pathways,” Journal of Biological Chemistry 293, no. 43 (2018): 16724–16740.

[261]

J. Jia, W. M. Zhao, X. Wang, M. Guo, and J. Sun, “Triptolide Impedes High Glucose-induced Cell Function in HK2 Cells Through PRKN-mediated Ubiquitination of ACSL1,” Journal of Endocrinology (2025), Published online November 26, JOE-25-0095.

[262]

Z. G. Zheng, Y. P. Zhang, X. Y. Zhang, et al., “Ergosterol Alleviates Hepatic Steatosis and Insulin Resistance via Promoting Fatty Acid β-oxidation by Activating Mitochondrial ACSL1,” Cell reports 44, no. 1 (2025): 115203.

[263]

T. Wang, Y. Dong, L. Yao, et al., “Adoptive Transfer of Metabolically Reprogrammed Macrophages for Atherosclerosis Treatment in Diabetic ApoE -/- mice,” Bioact Mater 16 (2022): 82–94.

[264]

T. Zhou, J. Xiong, X. Hu, et al., “Sec14L6 is a Phosphoinositide Transporter That Regulates Phosphoinositide Homeostasis and Biogenesis of Lipid Droplets,” Nature Communications 16, no. 1 (2025): 10518.

[265]

J. D. Griffin, Y. Zhu, A. Reeves, K. K. Buhman, and A. S. Greenberg, “Intestinal Acyl-CoA Synthetase 5 (ACSL5) Deficiency Potentiates Postprandial GLP-1 & PYY Secretion, Reduces Food Intake, and Protects Against Diet-induced Obesity,” Mol Metab 83 (2024): 101918.

[266]

Z. Wu, J. Sun, Z. Liao, et al., “An Update on the Therapeutic Implications of Long-chain Acyl-coenzyme A Synthetases in Nervous System Diseases,” Frontiers in neuroscience 16 (2022): 1030512.

[267]

A. L. Madsen, S. Bonàs-Guarch, S. Gheibi, et al., “Genetic Architecture of Oral Glucose-stimulated Insulin Release Provides Biological Insights Into Type 2 Diabetes Aetiology,” Nat Metab 6, no. 10 (2024): 1897–1912.

[268]

I. H. Ansari, M. J. Longacre, S. W. Stoker, et al., “Characterization of Acyl-CoA Synthetase Isoforms in Pancreatic Beta Cells: Gene Silencing Shows Participation of ACSL3 and ACSL4 in Insulin Secretion,” Arch Biochem Biophys 618 (2017): 32–43.

[269]

T. A. Bowman, K. R. O'Keeffe, T. D'Aquila, et al., “Acyl CoA Synthetase 5 (ACSL5) Ablation in Mice Increases Energy Expenditure and Insulin Sensitivity and Delays Fat Absorption,” Mol Metab 5, no. 3 (2016): 210–220.

[270]

Y. Xi, M. Yang, Z. Deng, et al., “ACSL5 promotes Lipid Deposition and Lipoapoptosis in Proximal Tubular Epithelial Cells of Diabetic Kidney Disease,” Molecular and Cellular Endocrinology 595 (2025): 112418.

[271]

J. Hong, X. Li, Y. Hao, et al., “The PRMT6/STAT1/ACSL1 Axis Promotes Ferroptosis in Diabetic Nephropathy,” Cell Death and Differentiation 31, no. 11 (2024): 1561–1575.

[272]

K. Hu, Z. Yu, Y. Yuan, et al., “Lactate/AARS1/H3K18la/LDHA Positive Feedback Loop Triggers Ferroptosis, Which Participates in Diabetic Nephropathy via the Modulation of ACSL4 Transcription,” Acta Biochim Biophys Sin (2025), Published online October 30.

[273]

Z. Chen, S. Li, M. Liu, et al., “Nicorandil Alleviates Cardiac Microvascular Ferroptosis in Diabetic Cardiomyopathy: Role of the Mitochondria-localized AMPK-Parkin-ACSL4 Signaling Pathway,” Pharmacological Research 200 (2024): 107057.

[274]

M. E. Rinella, J. V. Lazarus, V. Ratziu, et al., “A Multisociety Delphi Consensus Statement on New Fatty Liver Disease Nomenclature,” Hepatol Baltim Md 78, no. 6 (2023): 1966–1986.

[275]

Z. M. Younossi, P. Golabi, J. M. Paik, A. Henry, C. Van Dongen, and L. Henry, “The Global Epidemiology of Nonalcoholic Fatty Liver Disease (NAFLD) and Nonalcoholic Steatohepatitis (NASH): A Systematic Review,” Hepatol Baltim Md 77, no. 4 (2023): 1335–1347.

[276]

C. Estes, H. Razavi, R. Loomba, Z. Younossi, and A. J. Sanyal, “Modeling the Epidemic of Nonalcoholic Fatty Liver Disease Demonstrates an Exponential Increase in Burden of Disease,” Hepatol Baltim Md 67, no. 1 (2018): 123–133.

[277]

J. Quek, K. E. Chan, Z. Y. Wong, et al., “Global Prevalence of Non-alcoholic Fatty Liver Disease and Non-alcoholic Steatohepatitis in the Overweight and Obese Population: A Systematic Review and Meta-analysis,” Lancet Gastroenterol Hepatol 8, no. 1 (2023): 20–30.

[278]

E. En Li Cho, C. Z. Ang, J. Quek, et al., “Global Prevalence of Non-alcoholic Fatty Liver Disease in Type 2 Diabetes Mellitus: An Updated Systematic Review and Meta-analysis,” Gut 72, no. 11 (2023): 2138–2148.

[279]

Z. M. Younossi, A. B. Koenig, D. Abdelatif, Y. Fazel, L. Henry, and M. Wymer, “Global Epidemiology of Nonalcoholic Fatty Liver Disease-Meta-analytic Assessment of Prevalence, Incidence, and Outcomes,” Hepatol Baltim Md 64, no. 1 (2016): 73–84.

[280]

L. Xiang, X. Li, J. Gong, et al., “The Nomenclature of Fatty Liver Disease and Its Impact on Obesity Traits, Insulin Resistance, and Hepatic Fibrosis,” Lipids Health Dis 24, no. 1 (2025): 339.

[281]

G. Targher, L. Valenti, and C. D. Byrne, “Metabolic Dysfunction-Associated Steatotic Liver Disease,” New England Journal of Medicine 393, no. 7 (2025): 683–698.

[282]

D. H. Ipsen, J. Lykkesfeldt, and P. Tveden-Nyborg, “Molecular Mechanisms of Hepatic Lipid Accumulation in Non-alcoholic Fatty Liver Disease,” Cellular and molecular life sciences CMLS 75, no. 18 (2018): 3313–3327.

[283]

J. Westerbacka, M. Kolak, T. Kiviluoto, et al., “Genes Involved in Fatty Acid Partitioning and Binding, Lipolysis, Monocyte/Macrophage Recruitment, and Inflammation Are Overexpressed in the human Fatty Liver of Insulin-resistant Subjects,” Diabetes 56, no. 11 (2007): 2759–2765.

[284]

D. Greco, A. Kotronen, J. Westerbacka, et al., “Gene Expression in human NAFLD,” American journal of physiology Gastrointestinal and liver physiology 294, no. 5 (2008): G1281–1287.

[285]

C. G. Wilson, J. L. Tran, D. M. Erion, N. B. Vera, M. Febbraio, and E. J. Weiss, “Hepatocyte-Specific Disruption of CD36 Attenuates Fatty Liver and Improves Insulin Sensitivity in HFD-Fed Mice,” Endocrinology 157, no. 2 (2016): 570–585.

[286]

C. Zhou, Z. Shen, B. Shen, et al., “FABP4 in LSECs Promotes CXCL10-mediated Macrophage Recruitment and M1 Polarization During NAFLD Progression,” Biochim Biophys Acta Mol Basis Dis 1869, no. 7 (2023): 166810.

[287]

Y. Y. Yu, M. Feng, Y. Chen, et al., “Asprosin-FABP5 Interaction Modulates Mitochondrial Fatty Acid Oxidation Through PPARα Contributing to MASLD Development,” Advanced Science (Weinheim, Baden-Württemberg, Germany) 12, no. 21 (2025): e2415846.

[288]

Q. Zhang, J. Li, X. Liu, et al., “Inhibiting CD36 Palmitoylation Improves Cardiac Function Post-infarction by Regulating Lipid Metabolic Homeostasis and Autophagy,” Nature Communications 16, no. 1 (2025): 6602.

[289]

A. R. Terry, V. Nogueira, H. Rho, et al., “CD36 maintains Lipid Homeostasis via Selective Uptake of Monounsaturated Fatty Acids During Matrix Detachment and Tumor Progression,” Cell metabolism 35, no. 11 (2023): 2060–2076.e9.

[290]

J. Wang, J. Hu, H. Hu, et al., “APT1-derived Depalmitoylation of CD36 Alleviates Diabetes-induced Lipotoxicity in Podocytes,” Int J Biol Sci 21, no. 9 (2025): 3852–3866.

[291]

L. Zhao, C. Zhang, X. Luo, et al., “CD36 palmitoylation Disrupts Free Fatty Acid Metabolism and Promotes Tissue Inflammation in Non-alcoholic Steatohepatitis,” Journal of Hepatology 69, no. 3 (2018): 705–717.

[292]

D. Yang, L. Li, K. Zang, et al., “EVA1A Regulates Hepatic Lipid Homeostasis by Modulating CD36 Expression and Its Palmitoylation,” Res Wash DC 8 (2025): 1001.

[293]

Y. Wu, Z. Duan, L. Qu, Y. Liu, X. Ma, and D. Fan, “Ginsenoside Rk1 Ameliorates Non-Alcoholic Fatty Liver Disease by Targeting CD36 to Modulate the AMPK Signaling Pathway,” Food Research International (Ottawa, Ont) 211 (2025): 116426.

[294]

H. Zhu, T. Zhao, S. Zhao, et al., “O-GlcNAcylation Promotes the Progression of Nonalcoholic Fatty Liver Disease by Upregulating the Expression and Function of CD36,” Metabolism 156 (2024): 155914.

[295]

H. Li, Z. Li, L. Chen, et al., “PDHA1-mediated H3K18 Lactylation Is Involved in Arsenic-induced Nonalcoholic Fatty Liver Disease by Activating the CD36-NLRP3 Inflammasome Axis,” Journal of Hazardous Materials 498 (2025): 139852.

[296]

G. Mocciaro, M. Allison, B. Jenkins, et al., “Non-alcoholic Fatty Liver Disease Is Characterised by a Reduced Polyunsaturated Fatty Acid Transport via Free Fatty Acids and High-density Lipoproteins (HDL),” Molecular Metabolism 73 (2023): 101728.

[297]

Y. H. Fan, S. Zhang, Y. Wang, H. Wang, H. Li, and L. Bai, “Inter-organ Metabolic Interaction Networks in Non-alcoholic Fatty Liver Disease,” Front Endocrinol 15 (2024): 1494560.

[298]

V. Rosato, M. Masarone, M. Dallio, A. Federico, A. Aglitti, and M. Persico, “NAFLD and Extra-Hepatic Comorbidities: Current Evidence on a Multi-Organ Metabolic Syndrome,” International Journal of Environmental Research and Public Health 16, no. 18 (2019): 3415.

[299]

A. Mantovani, G. Petracca, G. Beatrice, et al., “Non-alcoholic Fatty Liver Disease and Risk of Incident Chronic Kidney Disease: An Updated Meta-analysis,” Gut 71, no. 1 (2022): 156–162.

[300]

G. Musso, M. Cassader, S. Cohney, S. Pinach, F. Saba, and R. Gambino, “Emerging Liver-Kidney Interactions in Nonalcoholic Fatty Liver Disease,” Trends in Molecular Medicine 21, no. 10 (2015): 645–662.

[301]

J. Rong, Z. Zhang, X. Peng, P. Li, T. Zhao, and Y. Zhong, “Mechanisms of Hepatic and Renal Injury in Lipid Metabolism Disorders in Metabolic Syndrome,” Int J Biol Sci 20, no. 12 (2024): 4783–4798.

[302]

L. Zhang, J. Wang, T. Xu, et al., “Bicyclol Alleviates Obesity-induced Renal Injury by Inhibiting JNK and NF-κB-mediated Inflammation,” International Immunopharmacology 129 (2024): 111609.

[303]

R. M. Wilechansky, A. Pedley, J. M. Massaro, U. Hoffmann, E. J. Benjamin, and M. T. Long, “Relations of Liver Fat With Prevalent and Incident Chronic Kidney Disease in the Framingham Heart Study: A Secondary Analysis,” Liver International: Official Journal of the International Association for the Study of the Liver 39, no. 8 (2019): 1535–1544.

[304]

B. Qi, V. Musale, X. Weng, et al., “A Novel Role of Hyaluronan and Its Membrane Receptors, CD44 and RHAMM, in Obesity-Related Kidney Pathology,” Biomolecules 15, no. 11 (2025): 1598.

[305]

Z. Chen, J. Liu, F. Zhou, et al., “Nonalcoholic Fatty Liver Disease: An Emerging Driver of Cardiac Arrhythmia,” Circulation Research 128, no. 11 (2021): 1747–1765.

[306]

K. Josloff, J. Beiriger, A. Khan, et al., “Comprehensive Review of Cardiovascular Disease Risk in Nonalcoholic Fatty Liver Disease,” Journal of Cardiovascular Development and Disease 9, no. 12 (2022): 419.

[307]

G. Styczynski, P. Kalinowski, Ł. Michałowski, et al., “Cardiac Morphology, Function, and Hemodynamics in Patients with Morbid Obesity and Nonalcoholic Steatohepatitis,” Journal of the American Heart Association 10, no. 8 (2021): e017371.

[308]

S. Wu, Q. Lu, Y. Ding, et al., “Hyperglycemia-Driven Inhibition of AMP-Activated Protein Kinase α2 Induces Diabetic Cardiomyopathy by Promoting Mitochondria-Associated Endoplasmic Reticulum Membranes in Vivo,” Circulation 139, no. 16 (2019): 1913–1936.

[309]

D. M. Radomska-Leśniewska, J. Niderla-Bielińska, M. Kujawa, and E. Jankowska-Steifer, “Targeting Metabolic Dysregulation in Obesity and Metabolic Syndrome: The Emerging Role of N-Acetylcysteine,” Metabolites 15, no. 10 (2025): 645.

[310]

B. Zhong, Z. Xie, J. Zhang, et al., “Identification of Key Genes Increasing Susceptibility to Atrial Fibrillation in Nonalcoholic Fatty Liver Disease and the Potential Mechanisms: Mitochondrial Dysfunction and Systemic Inflammation,” Frontiers in Pharmacology 15 (2024): 1360974.

[311]

G. Targher, A. Mantovani, C. Grander, et al., “Association Between Non-alcoholic Fatty Liver Disease and Impaired Cardiac Sympathetic/Parasympathetic Balance in Subjects With and Without Type 2 Diabetes-The Cooperative Health Research in South Tyrol (CHRIS)-NAFLD Sub-study,” Nutrition, Metabolism & Cardiovascular Diseases NMCD 31, no. 12 (2021): 3464–3473.

[312]

D. H. Sinn, D. Kang, M. Kang, et al., “Nonalcoholic Fatty Liver Disease and Accelerated Loss of Skeletal Muscle Mass: A Longitudinal Cohort Study,” Hepatol Baltim Md 76, no. 6 (2022): 1746–1754.

[313]

F. Li, H. S. Huang, Q. Zhao, et al., “Hepatic ASPG-mediated Lysophosphatidylinositol Catabolism Impairs Insulin Signal Transduction,” Embo Journal 44, no. 18 (2025): 5005–5036.

[314]

M. Tanaka, K. Kaji, N. Nishimura, et al., “Blockade of Angiotensin II Modulates Insulin-Like Growth Factor 1-mediated Skeletal Muscle Homeostasis in Experimental Steatohepatitis,” Biochimica et Biophysica Acta (BBA) - Molecular Cell Research 1871, no. 2 (2024): 119649.

[315]

S. Guo, Y. Feng, X. Zhu, et al., “Metabolic Crosstalk Between Skeletal Muscle Cells and Liver Through IRF4-FSTL1 in Nonalcoholic Steatohepatitis,” Nature Communications 14, no. 1 (2023): 6047.

[316]

L. Fan, D. R. Sweet, D. A. Prosdocimo, et al., “Muscle Krüppel-Like Factor 15 Regulates Lipid Flux and Systemic Metabolic Homeostasis,” Journal of Clinical Investigation 131, no. 4 (2021): e139496.

[317]

P. Libby, “The Changing Landscape of Atherosclerosis,” Nature 592, no. 7855 (2021): 524–533.

[318]

T. Bleckwehl, A. Babler, M. Tebens, et al., “Encompassing View of Spatial and Single-cell RNA Sequencing Renews the Role of the Microvasculature in human Atherosclerosis,” Nature Cardiovascular Research 4, no. 1 (2025): 26–44.

[319]

Y. X. Liu, F. M. Guo, W. J. Qiu, Y. P. Gao, X. Y. Han, and B. Shen, “Metabolic Reprogramming and Cell Interaction in Atherosclerosis: From Molecular Mechanisms to Therapeutic Strategies,” Journal of Cardiovascular Development and Disease 12, no. 10 (2025): 384.

[320]

A. Mastrangelo, I. Robles-Vera, D. Mañanes, et al., “Imidazole Propionate Is a Driver and Therapeutic Target in Atherosclerosis,” Nature 645, no. 8079 (2025): 254–261.

[321]

H. Bae, S. Jung, J. Le, et al., “Cross-organ Metabolite Production and Consumption in Healthy and Atherogenic Conditions,” Cell 188, no. 16 (2025): 4441–4455.e16.

[322]

M. Pibiri, A. Noto, A. Dalu, et al., “Metabolomics Signatures of Atherosclerosis in Cardiovascular Disease: A Narrative Systematic Review,” Journal of Clinical Medicine 14, no. 22 (2025): 8028.

[323]

K. De Bock, M. Georgiadou, S. Schoors, et al., “Role of PFKFB3-driven Glycolysis in Vessel Sprouting,” Cell 154, no. 3 (2013): 651–663.

[324]

X. Zhu, Y. Wang, I. Soaita, et al., “Acetate Controls Endothelial-to-mesenchymal Transition,” Cell metabolism 35, no. 7 (2023): 1163–1178.e10.

[325]

A. Pasut, E. Lama, A. H. Van Craenenbroeck, J. Kroon, and P. Carmeliet, “Endothelial Cell Metabolism in Cardiovascular Physiology and Disease,” Nature Reviews Cardiology 22, no. 12 (2025): 923–943.

[326]

Y. Dai, C. V. C. Junho, L. Schieren, et al., “Cellular Metabolism Changes in Atherosclerosis and the Impact of Comorbidities,” Frontiers in Cell and Developmental Biology 12 (2024): 1446964.

[327]

M. Cao, M. Li, X. Li, et al., “Endothelial Soluble Epoxide Hydrolase Links Polyunsaturated Fatty Acid Metabolism to Oxidative Stress and Atherosclerosis Progression,” Redox Biology 85 (2025): 103730.

[328]

L. He, Q. Chen, L. Wang, et al., “Activation of Nrf2 Inhibits Atherosclerosis in ApoE-/- mice Through Suppressing Endothelial Cell Inflammation and Lipid Peroxidation,” Redox Biology 74 (2024): 103229.

[329]

L. F. He, L. Wang, J. W. Li, et al., “Endothelial Gsα Deficiency Promotes Ferroptosis and Exacerbates Atherosclerosis in Apolipoprotein E-deficient Mice via the Inhibition of NRF2 Signaling,” Acta Pharmacologica Sinica 46, no. 5 (2025): 1289–1302.

[330]

Y. Lv, X. Weng, Y. Zhu, et al., “Quercetin Alleviates Postmenopausal Atherosclerosis by Suppressing Endothelial Cell Ferroptosis via Regulating the KEAP1/NRF2/GPX4 Signalling Pathway,” British Journal of Pharmacology (2025), Published online October 8.

[331]

S. Wang, X. Song, H. Gao, Y. Zhang, X. Zhou, and F. Wang, “6-Gingerol Inhibits Ferroptosis in Endothelial Cells in Atherosclerosis by Activating the NRF2/HO-1 Pathway,” Applied Biochemistry and Biotechnology 197, no. 6 (2025): 3890–3906.

[332]

Y. Q. Wu, R. M. Wu, Y. Zeng, and X. Le Xu, “Nrf2-mediated Inhibition of Ferroptosis Contributes to the Amelioration of Atherosclerosis by Polydatin,” Toxicology and Applied Pharmacology 504 (2025): 117538.

[333]

M. Zheng, F. Zhang, X. Gong, and H. Yuan, “Ginseng Peptide Extract Alleviates Nicotine-induced Oxidative Stress and Apoptosis in human Aortic Endothelial Cells by Preserving the Balance of the Keap1/Nrf2/HO-1 Signaling Pathway,” International Immunopharmacology 159 (2025): 114901.

[334]

H. Yang, S. E. Lee, S. I. Jeong, C. S. Park, Y. H. Jin, and Y. S. Park, “Up-regulation of Heme Oxygenase-1 by Korean Red Ginseng Water Extract as a Cytoprotective Effect in Human Endothelial Cells,” Journal of Ginseng Research 35, no. 3 (2011): 352–359.

[335]

S. Huang, Z. Liu, H. Liu, et al., “Nepeta Angustifolia Attenuates Responses to Vascular Inflammation in High Glucose-induced human Umbilical Vein Endothelial Cells Through Heme Oxygenase-1 Induction,” Journal of Ethnopharmacology 231 (2019): 187–196.

[336]

X. Cai, Y. Zhang, W. Zhu, and N. Gu, “Kaempferol inhibits atherosclerotic plaque development via dual-targeting of p53-p21-p16 senescence Pathway and Nrf2/HO-1/NQO1 Antioxidant Mechanism: Insights From Combined in Vivo and in Vitro Research,” International Immunopharmacology 166 (2025): 115587.

[337]

Y. J. Kuang, Q. Q. Chen, J. H. Hao, Y. Lin, P. T. Xiao, and E. H. Liu, “Typhae Pollen Attenuates Atherosclerosis by Enhancing Vascular Endothelium Function and Lipid Metabolism,” Journal of Ethnopharmacology 355, no. Pt A (2026): 120604.

[338]

I. Tabas and K. E. Bornfeldt, “Macrophage Phenotype and Function in Different Stages of Atherosclerosis,” Circulation Research 118, no. 4 (2016): 653–667.

[339]

K. J. Moore, F. J. Sheedy, and E. A. Fisher, “Macrophages in Atherosclerosis: A Dynamic Balance,” Nature Reviews Immunology 13, no. 10 (2013): 709–721.

[340]

T. Li, X. Gu, X. Yin, et al., “Macrophage Phospholipase D3 Promotes Atherosclerosis via Exacerbating Foam Cell Formation and Inducing Inflammatory Responses,” IJC Heart & Vasculature 61 (2025): 101834.

[341]

J. Wang, L. Peng, H. Wang, et al., “Regulation of Lipoprotein Processing by GPNMB in Foamy Macrophages: Potential Therapeutic Targets for Atherosclerosis,” Nature Communications 16, no. 1 (2025): 10030.

[342]

F. Fang, E. Wang, H. Yang, et al., “Reprogramming Mitochondrial Metabolism and Epigenetics of Macrophages via miR-10a Liposomes for Atherosclerosis Therapy,” Nature Communications 16, no. 1 (2025): 9117.

[343]

X. Wei, H. Song, L. Yin, et al., “Fatty Acid Synthesis Configures the Plasma Membrane for Inflammation in Diabetes,” Nature 539, no. 7628 (2016): 294–298.

[344]

R. Meade, D. Ibrahim, C. Engel, et al., “Targeting Fatty Acid Synthase Reduces Aortic Atherosclerosis and Inflammation,” Communications Biology 8, no. 1 (2025): 262.

[345]

G. Y. Peng, L. T. Wei, Y. X. Jing, et al., “TMEM41B contributes to Atherosclerosis by Promoting Lipid Synthesis in Vascular Smooth Muscle Cells via Fatty Acid Synthase Stabilization,” Metabolism 175 (2026): 156456.

[346]

P. Swiatlowska, W. Tipping, E. Marhuenda, et al., “Hypertensive Pressure Mechanosensing Alone Triggers Lipid Droplet Accumulation and Transdifferentiation of Vascular Smooth Muscle Cells to Foam Cells,” Adv Sci Weinh Baden-Wurtt Ger 11, no. 9 (2024): e2308686.

[347]

J. Guo and L. Du, “An Update on Ox-LDL-inducing Vascular Smooth Muscle Cell-derived Foam Cells in Atherosclerosis,” Frontiers in Cell and Developmental Biology 12 (2024): 1481505.

[348]

GBD 2019 Dementia Forecasting Collaborators. Estimation of the Global Prevalence of Dementia in 2019 and Forecasted Prevalence in 2050: An Analysis for the Global Burden of Disease Study 2019. Lancet Public Health 2022; 7(2): e105–e125.

[349]

S. E. Mackey-Alfonso and R. M. Barrientos, “Neuroinflammatory Mechanisms Linking High-fat Diets to Alzheimer's Disease Vulnerability: Beyond the Amyloid Hypothesis,” Alzheimers Dement J Alzheimers Assoc 21, no. 11 (2025): e70911.

[350]

N. Mota-Martorell, P. Andrés-Benito, M. Martín-Gari, et al., “Selective Brain Regional Changes in Lipid Profile With human Aging,” GeroScience 44, no. 2 (2022): 763–783.

[351]

M. Moreno-Rodriguez, S. E. Perez, J. Martinez-Gardeazabal, et al., “Frontal Cortex Lipid Alterations during the Onset of Alzheimer's Disease,” J Alzheimers Dis JAD 98, no. 4 (2024): 1515–1532.

[352]

J. Lee, J. M. Dimitry, J. H. Song, et al., “Microglial REV-ERBα Regulates Inflammation and Lipid Droplet Formation to Drive Tauopathy in Male Mice,” Nature Communications 14, no. 1 (2023): 5197.

[353]

J. F. Kuehn, Q. Zhang, M. B. Heston, et al., “Fecal Short-chain Fatty Acids Vary by Sex and Amyloid Status,” Alzheimers Dement J Alzheimers Assoc 21, no. 11 (2025): e70877.

[354]

S. Chandra, J. Popovic, N. K. Singhal, et al., “The Gut Microbiome Controls Reactive Astrocytosis During Aβ Amyloidosis via Propionate-mediated Regulation of IL-17,” Journal of Clinical Investigation 135, no. 13 (2025): e180826.

[355]

J. Wang, J. Xie, F. He, et al., “Akkermansia Muciniphila-derived SCFAs Improve the Depression-Like Behaviors of Mice by Inhibiting Neuroinflammation,” Pharmacological Research 220 (2025): 107938.

[356]

R. Yu, H. Zhang, R. Chen, et al., “Fecal Microbiota Transplantation From Methionine-Restricted Diet Mouse Donors Improves Alzheimer's Learning and Memory Abilities through Short-Chain Fatty Acids,” Foods Basel Switz 14, no. 1 (2025): 101.

[357]

S. D. Reddy, B. L. Clossen, and D. S. Reddy, “Epigenetic Histone Deacetylation Inhibition Prevents the Development and Persistence of Temporal Lobe Epilepsy,” Journal of Pharmacology and Experimental Therapeutics 364, no. 1 (2018): 97–109.

[358]

Y. Li, D. Munoz-Mayorga, Y. Nie, et al., “Microglial Lipid Droplet Accumulation in Tauopathy Brain Is Regulated by Neuronal AMPK,” Cell metabolism 36, no. 6 (2024): 1351–1370.e8.

[359]

M. S. Haney, R. Pálovics, C. N. Munson, et al., “APOE4/4 is Linked to Damaging Lipid Droplets in Alzheimer's Disease Microglia,” Nature 628, no. 8006 (2024): 154–161.

[360]

X. Wu, J. A. Miller, B. T. K. Lee, Y. Wang, and C. Ruedl, “Reducing Microglial Lipid Load Enhances β Amyloid Phagocytosis in an Alzheimer's Disease Mouse Model,” Science Advances 11, no. 6 (2025): eadq6038.

[361]

P. Prakash, P. Manchanda, E. Paouri, et al., “Amyloid-β Induces Lipid Droplet-mediated Microglial Dysfunction via the Enzyme DGAT2 in Alzheimer's Disease,” Immunity 58, no. 6 (2025): 1536–1552.e8.

[362]

J. Marschallinger, T. Iram, M. Zardeneta, et al., “Lipid-droplet-accumulating Microglia Represent a Dysfunctional and Proinflammatory state in the Aging Brain,” Nature Neuroscience 23, no. 2 (2020): 194–208.

[363]

X. Zhao, X. Yang, C. Du, et al., “Up-regulated Succinylation Modifications Induce a Senescence Phenotype in Microglia by Altering Mitochondrial Energy Metabolism,” Journal of Neuroinflammation 21, no. 1 (2024): 296.

[364]

M. Gao, J. Bai, F. Lou, et al., “Loss of MFE-2 Impairs Microglial Lipid Homeostasis and Drives Neuroinflammation in Alzheimer's Pathogenesis,” Nature Aging 5, no. 11 (2025): 2279–2296.

[365]

Q. Li, P. Liu, X. Zhu, et al., “NG-497 Alleviates Microglia-Mediated Neuroinflammation in a MTNR1A-Dependent Manner,” Inflammation 48, no. 4 (2025): 2663–2676.

[366]

F. Van Gaever, F. Mingneau, S. Vanherle, et al., “The Phytohormone Abscisic Acid Enhances Remyelination in Mouse Models of Multiple Sclerosis,” Frontiers in immunology 15 (2024): 1500697.

[367]

D. Guo, S. Cai, L. Deng, et al., “Ferroptosis in Pulmonary Disease and Lung Cancer: Molecular Mechanisms, Crosstalk Regulation, and Therapeutic Strategies,” MedComm 6, no. 3 (2025): e70116.

[368]

E. Currie, A. Schulze, R. Zechner, T. C. Walther, and R. V. Farese, “Cellular Fatty Acid Metabolism and Cancer,” Cell metabolism 18, no. 2 (2013): 153–161.

[369]

L. Zhang, Y. Yao, and S. Liu, “Targeting Fatty Acid Metabolism for Cancer Therapy,” Fundam Res (2024), Published online September 28.

[370]

Y. Lu, Y. Wang, T. Ruan, et al., “Immunometabolism of Tregs: Mechanisms, Adaptability, and Therapeutic Implications in Diseases,” Frontiers in immunology 16 (2025): 1536020.

[371]

S. Siddiqui and R. Glauben, “Fatty Acid Metabolism in Myeloid-Derived Suppressor Cells and Tumor-Associated Macrophages: Key Factor in Cancer Immune Evasion,” Cancers 14, no. 1 (2022): 250.

[372]

R. L. Silverstein and M. Febbraio, “CD36, a Scavenger Receptor Involved in Immunity, Metabolism, Angiogenesis, and Behavior,” Science signaling 2, no. 72 (2009): re3.

[373]

O. Kuda, T. A. Pietka, Z. Demianova, et al., “Sulfo-N-succinimidyl Oleate (SSO) Inhibits Fatty Acid Uptake and Signaling for Intracellular Calcium via Binding CD36 Lysine 164: SSO Also Inhibits Oxidized Low Density Lipoprotein Uptake by Macrophages,” Journal of Biological Chemistry 288, no. 22 (2013): 15547–15555.

[374]

M. Takaichi, H. Tachinami, D. Takatsuka, et al., “Targeting CD36-Mediated Lipid Metabolism by Selective Inhibitor-Augmented Antitumor Immune Responses in Oral Cancer,” International Journal of Molecular Sciences 25, no. 17 (2024): 9438.

[375]

H. Wang, F. Liu, X. Wu, et al., “Cancer-associated Fibroblasts Contributed to Hepatocellular Carcinoma Recurrence and Metastasis via CD36-mediated Fatty-acid Metabolic Reprogramming,” Experimental Cell Research 435, no. 2 (2024): 113947.

[376]

H. Dhungana, M. T. Huuskonen, M. Jaronen, et al., “Sulfosuccinimidyl Oleate Sodium Is Neuroprotective and Alleviates Stroke-induced Neuroinflammation,” Journal of Neuroinflammation 14, no. 1 (2017): 237.

[377]

J. Qu, D. Li, J. Jin, et al., “Hypoxia-Inducible Factor 2α Attenuates Renal Ischemia-Reperfusion Injury by Suppressing CD36-Mediated Lipid Accumulation in Dendritic Cells in a Mouse Model,” J Am Soc Nephrol JASN 34, no. 1 (2023): 73–87.

[378]

B. N. Wang, A. Y. Du, X. H. Chen, et al., “Inhibition of CD36 Ameliorates Mouse Spinal Cord Injury by Accelerating Microglial Lipophagy,” Acta Pharmacologica Sinica (2025), Published online January 29.

[379]

J. A. Menendez and R. Lupu, “Fatty Acid Synthase and the Lipogenic Phenotype in Cancer Pathogenesis,” Nature Reviews Cancer 7, no. 10 (2007): 763–777.

[380]

R. Bai and J. Cui, “Regulation of Fatty Acid Synthase on Tumor and Progress in the Development of Related Therapies,” Chinese Medical Journal 137, no. 16 (2024): 1894–1902.

[381]

J. A. Menendez, E. Cuyàs, J. A. Encinar, et al., “Fatty Acid Synthase (FASN) Signalome: A Molecular Guide for Precision Oncology,” Mol Oncol 18, no. 3 (2024): 479–516.

[382]

A. Schcolnik-Cabrera, A. Chávez-Blanco, G. Domínguez-Gómez, et al., “Orlistat as a FASN Inhibitor and Multitargeted Agent for Cancer Therapy,” Expert Opinion on Investigational Drugs 27, no. 5 (2018): 475–489.

[383]

J. Ye, Y. Wu, F. Li, et al., “Effect of orlistat on Liver Fat Content in Patients With Nonalcoholic Fatty Liver Disease With Obesity: Assessment Using Magnetic Resonance Imaging-derived Proton Density Fat Fraction,” Ther Adv Gastroenterol 12 (2019): 1756284819879047.

[384]

A. Zahmatkesh, M. H. Sohouli, S. Shojaie, and P. Rohani, “The Effect of Orlistat in the Treatment of Non-alcoholic Fatty Liver in Adolescents With Overweight and Obese,” European Journal of Pediatrics 183, no. 3 (2024): 1173–1182.

[385]

E. Polonio-Alcalá, R. Porta, S. Ruiz-Martínez, et al., “AZ12756122, a Novel Fatty Acid Synthase Inhibitor, Decreases Resistance Features in EGFR-TKI Resistant EGFR-mutated NSCLC Cell Models,” Biomed Pharmacother Biomedecine Pharmacother 156 (2022): 113942.

[386]

M. O'Farrell, G. Duke, and R. Crowley, “FASN Inhibition Targets Multiple Drivers of NASH by Reducing Steatosis, Inflammation and Fibrosis in Preclinical models,” in Sci Rep (2022), 15661.

[387]

L. Y. Chen, D. S. Wu, and Y. A. Shen, “Fatty Acid Synthase Inhibitor Cerulenin Hinders Liver Cancer Stem Cell Properties Through FASN/APP Axis as Novel Therapeutic Strategies,” Journal of Lipid Research 65, no. 11 (2024): 100660.

[388]

L. Chen, Y. Duan, H. Wei, et al., “Acetyl-CoA Carboxylase (ACC) as a Therapeutic Target for Metabolic Syndrome and Recent Developments in ACC1/2 Inhibitors,” Expert Opinion on Investigational Drugs 28, no. 10 (2019): 917–930.

[389]

G. Harriman, J. Greenwood, S. Bhat, et al., “Acetyl-CoA Carboxylase Inhibition by ND-630 Reduces Hepatic Steatosis, Improves Insulin Sensitivity, and Modulates Dyslipidemia in Rats,” PNAS 113, no. 13 (2016): E1796–1805.

[390]

L. Goedeke, J. Bates, D. F. Vatner, et al., “Acetyl-CoA Carboxylase Inhibition Reverses NAFLD and Hepatic Insulin Resistance but Promotes Hypertriglyceridemia in Rodents,” Hepatol Baltim Md 68, no. 6 (2018): 2197–2211.

[391]

T. T. Ross, C. Crowley, K. L. Kelly, et al., “Acetyl-CoA Carboxylase Inhibition Improves Multiple Dimensions of NASH Pathogenesis in Model Systems,” Cell Mol Gastroenterol Hepatol 10, no. 4 (2020): 829–851.

[392]

E. Q. Li, W. Zhao, C. Zhang, et al., “Synthesis and Anti-cancer Activity of ND-646 and Its Derivatives as Acetyl-CoA Carboxylase 1 Inhibitors,” Eur J Pharm Sci Off J Eur Fed Pharm Sci 137 (2019): 105010.

[393]

R. U. Svensson, S. J. Parker, L. J. Eichner, et al., “Inhibition of Acetyl-CoA Carboxylase Suppresses Fatty Acid Synthesis and Tumor Growth of Non-small-cell Lung Cancer in Preclinical Models,” Nature Medicine 22, no. 10 (2016): 1108–1119.

[394]

J. S. V. Lally, S. Ghoshal, D. K. DePeralta, et al., “Inhibition of Acetyl-CoA Carboxylase by Phosphorylation or the Inhibitor ND-654 Suppresses Lipogenesis and Hepatocellular Carcinoma,” Cell metabolism 29, no. 1 (2019): 174–182.e5.

[395]

Q. Chu, J. An, P. Liu, et al., “Repurposing a Tricyclic Antidepressant in Tumor and Metabolism Disease Treatment Through Fatty Acid Uptake Inhibition,” Journal of Experimental Medicine 220, no. 3 (2023): e20221316.

[396]

S. Cheng, G. Wang, Y. Wang, et al., “Fatty Acid Oxidation Inhibitor etomoxir Suppresses Tumor Progression and Induces Cell Cycle Arrest via PPARγ-mediated Pathway in Bladder Cancer,” Clin Sci Lond Engl 1979 133, no. 15 (2019): 1745–1758.

[397]

S. Kant, P. Kesarwani, A. R. Guastella, et al., “Perhexiline Demonstrates FYN-mediated Anti-tumor Activity in Glioblastoma,” Molecular Cancer Therapeutics 19, no. 7 (2020): 1415–1422.

[398]

A. Hu, H. Wang, Q. Xu, et al., “A Novel CPT1A Covalent Inhibitor Modulates Fatty Acid Oxidation and CPT1A-VDAC1 Axis With Therapeutic Potential for Colorectal Cancer,” Redox Biology 68 (2023): 102959.

[399]

R. Dashnamoorthy, F. Lansigan, W. L. Davis, W. B. Kinlaw, R. Gartenhaus, and A. M. Evens, “Targeting the Interactions of Fatty Acid Metabolism with PI3K/mTOR and MAPK as a Novel Therapeutic Strategy in Diffuse Large B-Cell Lymphoma (DLBCL),” Blood 122, no. 21 (2013): 5133–5133.

[400]

J. Seo, D. W. Jeong, J. W. Park, K. W. Lee, J. Fukuda, and Y. S. Chun, “Fatty-acid-induced FABP5/HIF-1 Reprograms Lipid Metabolism and Enhances the Proliferation of Liver Cancer Cells,” Communications Biology 3, no. 1 (2020): 638.

[401]

Y. Chen, X. Xu, Y. Wang, et al., “Hypoxia-induced SKA3 Promoted Cholangiocarcinoma Progression and Chemoresistance by Enhancing Fatty Acid Synthesis via the Regulation of PAR-dependent HIF-1a Deubiquitylation,” Journal of Experimental & Clinical Cancer Research 42, no. 1 (2023): 265.

[402]

Y. Mo, Y. Han, Y. Chen, et al., “ZDHHC20 mediated S-palmitoylation of Fatty Acid Synthase (FASN) Promotes Hepatocarcinogenesis,” Molecular Cancer 23, no. 1 (2024): 274.

[403]

M. Ye, C. Hu, T. Chen, et al., “FABP5 suppresses Colorectal Cancer Progression via mTOR-mediated Autophagy by Decreasing FASN Expression,” International Journal of Biological Sciences 19, no. 10 (2023): 3115–3127.

[404]

B. L. Horton and S. Spranger, “CD36 - the Achilles' heel of Treg Cells,” Nature Immunology 21, no. 3 (2020): 251–253.

[405]

J. Gyamfi, J. H. Yeo, D. Kwon, et al., “Interaction Between CD36 and FABP4 Modulates Adipocyte-induced Fatty Acid Import and Metabolism in Breast Cancer,” NPJ Breast Cancer 7, no. 1 (2021): 129.

[406]

J. Guo, H. Gu, S. Yin, et al., “Hepatocyte-derived Igκ Promotes HCC Progression by Stabilizing Electron Transfer Flavoprotein Subunit α to Facilitate Fatty Acid β-oxidation,” Journal of Experimental & Clinical Cancer Research 43, no. 1 (2024): 280.

[407]

J. K. Patra, G. Das, L. F. Fraceto, et al., “Nano Based Drug Delivery Systems: Recent Developments and Future Prospects,” Journal of Nanobiotechnology 16, no. 1 (2018): 71.

[408]

W. Hou, W. Hong, S. Cai, et al., “RRM2-targeted Nanocarrier Enhances Radiofrequency Ablation Efficacy in Hepatocellular Carcinoma Through Ferroptosis Amplification and Immune Remodeling,” iMeta 4, no. 5 (2025): e70067.

[409]

Y. Zhou, J. Yuan, K. Xu, S. Li, and Y. Liu, “Nanotechnology Reprogramming Metabolism for Enhanced Tumor Immunotherapy,” ACS Nano 18, no. 3 (2024): 1846–1864.

[410]

M. Ma, Y. Zhang, K. Pu, and W. Tang, “Nanomaterial-enabled Metabolic Reprogramming Strategies for Boosting Antitumor Immunity,” Chemical Society Reviews 54, no. 2 (2025): 653–714.

[411]

R. Li, Y. Li, Z. Song, et al., “A Graphene-Based Lipid Modulation Nanoplatform for Synergetic Lipid Starvation/Chemo/Photothermal Therapy of Oral Squamous Cell Carcinoma,” International Journal of Nanomedicine 19 (2024): 11235–11255.

[412]

M. Jiang, X. Li, J. Zhang, et al., “Dual Inhibition of Endoplasmic Reticulum Stress and Oxidation Stress Manipulates the Polarization of Macrophages Under Hypoxia to Sensitize Immunotherapy,” ACS Nano 15, no. 9 (2021): 14522–14534.

[413]

A. Ramesh, V. Malik, A. Brouillard, and A. Kulkarni, “Supramolecular Nanotherapeutics Enable Metabolic Reprogramming of Tumor-associated Macrophages to Inhibit Tumor Growth,” Journal of Biomedical Materials Research Part A 110, no. 8 (2022): 1448–1459.

[414]

D. Kim, Y. Wu, Q. Li, and Y. K. Oh, “Nanoparticle-Mediated Lipid Metabolic Reprogramming of T Cells in Tumor Microenvironments for Immunometabolic Therapy,” Nano-Micro Lett 13, no. 1 (2021): 31.

[415]

Y. Gao, Z. Song, L. Jia, et al., “Self-amplified ROS Production From Fatty Acid Oxidation Enhanced Tumor Immunotherapy by Atorvastatin/PD-L1 siRNA Lipopeptide Nanoplexes,” Biomaterials 291 (2022): 121902.

[416]

X. He, T. Deng, J. Li, et al., “A Core-satellite Micellar System Against Primary Tumors and Their Lymphatic Metastasis Through Modulation of Fatty Acid Metabolism Blockade and Tumor-associated Macrophages,” Nanoscale 15, no. 18 (2023): 8320–8336.

[417]

S. Cao, P. E. Saw, Q. Shen, R. Li, Y. Liu, and X. Xu, “Reduction-responsive RNAi Nanoplatform to Reprogram Tumor Lipid Metabolism and Repolarize Macrophage for Combination Pancreatic Cancer Therapy,” Biomaterials 280 (2022): 121264.

[418]

D. P. Rose and J. M. Connolly, “Omega-3 Fatty Acids as Cancer Chemopreventive Agents,” Pharmacology & Therapeutics 83, no. 3 (1999): 217–244.

[419]

W. E. Hardman, “Omega-3 Fatty Acids to Augment Cancer Therapy,” Journal of Nutrition 132, no. 11 Suppl (2002): 3508S–3512S.

[420]

L. A. Davidson, D. V. Nguyen, R. M. Hokanson, et al., “Chemopreventive n -3 Polyunsaturated Fatty Acids Reprogram Genetic Signatures During Colon Cancer Initiation and Progression in the Rat,” Cancer Research 64, no. 18 (2004): 6797–6804.

[421]

P. D. Schley, H. B. Jijon, L. E. Robinson, and C. J. Field, “Mechanisms of Omega-3 Fatty Acid-induced Growth Inhibition in MDA-MB-231 human Breast Cancer Cells,” Breast Cancer Research and Treatment 92, no. 2 (2005): 187–195.

[422]

C. A. C. Hyde and S. Missailidis, “Inhibition of Arachidonic Acid Metabolism and Its Implication on Cell Proliferation and Tumour-angiogenesis,” International Immunopharmacology 9, no. 6 (2009): 701–715.

[423]

L. Spencer, C. Mann, M. Metcalfe, et al., “The Effect of Omega-3 FAs on Tumour Angiogenesis and Their Therapeutic Potential,” Eur J Cancer Oxf Engl 1990 45, no. 12 (2009): 2077–2086.

[424]

S. F. Nabavi, S. Bilotto, G. L. Russo, et al., “Omega-3 Polyunsaturated Fatty Acids and Cancer: Lessons Learned From Clinical Trials,” Cancer and Metastasis Reviews 34, no. 3 (2015): 359–380.

[425]

J. de Aguiar Pastore Silva, M. Emilia de Souza Fabre, and D. L. Waitzberg, “Omega-3 Supplements for Patients in Chemotherapy and/or Radiotherapy: A Systematic Review,” Clin Nutr Edinb Scotl 34, no. 3 (2015): 359–366.

[426]

P. A. Corsetto, I. Colombo, J. Kopecka, A. M. Rizzo, and C. Riganti, “Long Chain Polyunsaturated Fatty Acids as Sensitizing Agents and Multidrug Resistance Revertants in Cancer Therapy,” International Journal of Molecular Sciences 18, no. 12 (2017): 2770.

[427]

B. M. Morsy, S. El Domiaty, M. A. M. Meheissen, L. A. Heikal, M. A. Meheissen, and N. M. Aly, “Omega-3 Nanoemulgel in Prevention of Radiation-induced Oral Mucositis and Its Associated Effect on Microbiome: A Randomized Clinical Trial,” BMC Oral Health 23, no. 1 (2023): 612.

[428]

M. Murray, “Omega-3 Polyunsaturated Fatty Acid Derived Lipid Mediators: A Comprehensive Update on Their Application in Anti-cancer Drug Discovery,” Expert Opinion on Drug Discovery 19, no. 5 (2024): 617–629.

[429]

K. L. Fritsche, “The Science of Fatty Acids and Inflammation,” Adv Nutr Bethesda Md 6, no. 3 (2015): 293S–301S.

[430]

F. Shahidi and P. Ambigaipalan, “Omega-3 Polyunsaturated Fatty Acids and Their Health Benefits,” Annual Review of Food Science and Technology 9 (2018): 345–381.

[431]

P. Fedele, A. N. Santoro, F. Pini, et al., “Immunonutrition, Metabolism, and Programmed Cell Death in Lung Cancer: Translating Bench to Bedside,” Biology 13, no. 6 (2024): 409.

[432]

L. A. de van der Schueren MAE, H. Blanchard, M. Jourdan, J. Arends, and V. E. Baracos, “Systematic Review and Meta-analysis of the Evidence for Oral Nutritional Intervention on Nutritional and Clinical Outcomes During Chemo(radio)Therapy: Current Evidence and Guidance for Design of Future Trials,” Annals of Oncology: Official Journal of the European Society for Medical Oncology 29, no. 5 (2018): 1141–1153.

[433]

Y. Zhang, Y. Sun, S. Song, et al., “Associations of Plasma Omega-6 and Omega-3 Fatty Acids With Overall and 19 Site-specific Cancers: A Population-based Cohort Study in UK Biobank,” International Journal of Cancer (2024), Published online October 17.

[434]

K. Walter, S. M. Hong, S. Nyhan, et al., “Serum Fatty Acid Synthase as a Marker of Pancreatic Neoplasia,” Cancer Epidemiol Biomark Prev Publ Am Assoc Cancer Res Cosponsored Am Soc Prev Oncol 18, no. 9 (2009): 2380–2385.

[435]

D. Buckley, G. Duke, T. S. Heuer, et al., “Fatty Acid Synthase—Modern Tumor Cell Biology Insights Into a Classical Oncology Target,” Pharmacology & Therapeutics 177 (2017): 23–31.

[436]

Y. Yu, Q. Nie, Z. Wang, Y. Di, X. Chen, and K. Ren, “Targeting Acetyl-CoA Carboxylase 1 for Cancer Therapy,” Frontiers in Pharmacology 14 (2023): 1129010.

[437]

P. Icard, Z. Wu, L. Fournel, A. Coquerel, H. Lincet, and M. Alifano, “ATP Citrate Lyase: A Central Metabolic Enzyme in Cancer,” Cancer Letters 471 (2020): 125–134.

[438]

J. Quan, A. M. Bode, and X. Luo, “ACSL Family: The Regulatory Mechanisms and Therapeutic Implications in Cancer,” European Journal of Pharmacology 909 (2021): 174397.

[439]

U. D. Orlando, A. F. Castillo, M. A. R. Medrano, A. R. Solano, P. M. Maloberti, and E. J. Podesta, “Acyl-CoA Synthetase-4 Is Implicated in Drug Resistance in Breast Cancer Cell Lines Involving the Regulation of Energy-dependent Transporter Expression,” Biochemical Pharmacology 159 (2019): 52–63.

[440]

M. Rossi Sebastiano and G. Konstantinidou, “Targeting Long Chain Acyl-CoA Synthetases for Cancer Therapy,” International Journal of Molecular Sciences 20, no. 15 (2019): 3624.

[441]

Y. Yang, T. Zhu, X. Wang, et al., “ACSL3 and ACSL4, Distinct Roles in Ferroptosis and Cancers,” Cancers 14, no. 23 (2022): 5896.

[442]

J. Hou, C. Jiang, X. Wen, et al., “ACSL4 as a Potential Target and Biomarker for Anticancer: From Molecular Mechanisms to Clinical Therapeutics,” Frontiers in pharmacology 13 (2022): 949863.

[443]

J. Lin, Y. Lai, F. Lu, and W. Wang, “Targeting ACSLs to Modulate Ferroptosis and Cancer Immunity,” Trends in Endocrinology & Metabolism S1043-2760, no. 24 (2024): 00255–00258, Published online October 17.

[444]

W. C. Chen, C. Y. Wang, Y. H. Hung, T. Y. Weng, M. C. Yen, and M. D. Lai, “Systematic Analysis of Gene Expression Alterations and Clinical Outcomes for Long-Chain Acyl-Coenzyme A Synthetase Family in Cancer,” PLoS ONE 11, no. 5 (2016): e0155660.

[445]

Q. Zhang, W. Zhou, S. Yu, et al., “Metabolic Reprogramming of Ovarian Cancer Involves ACSL1-mediated Metastasis Stimulation Through Upregulated Protein Myristoylation,” Oncogene 40, no. 1 (2021): 97–111.

[446]

Y. Ma, M. Nenkov, A. Berndt, et al., “The Diagnostic Value of ACSL1, ACSL4, and ACSL5 and the Clinical Potential of an ACSL Inhibitor in Non-Small-Cell Lung Cancer,” Cancers 16, no. 6 (2024): 1170.

[447]

Y. Yang, J. Liang, J. Zhao, et al., “The Multi-omics Analyses of acsl1 Reveal Its Translational Significance as a Tumor Microenvironmental and Prognostic Biomarker in Clear Cell Renal Cell Carcinoma,” Diagnostic Pathology 18, no. 1 (2023): 96.

[448]

L. P. Fernández, M. Merino, G. Colmenarejo, et al., “Metabolic Enzyme ACSL3 Is a Prognostic Biomarker and Correlates With Anticancer Effectiveness of Statins in Non-small Cell Lung Cancer,” Molecular Oncology 14, no. 12 (2020): 3135–3152.

[449]

X. Wu, Y. Li, J. Wang, et al., “Long Chain Fatty Acyl-CoA Synthetase 4 Is a Biomarker for and Mediator of Hormone Resistance in human Breast Cancer,” PLoS ONE 8, no. 10 (2013): e77060.

[450]

F. Hartmann, D. Sparla, E. Tute, et al., “Low Acyl-CoA Synthetase 5 Expression in Colorectal Carcinomas Is Prognostic for Early Tumour Recurrence,” Pathology, Research and Practice 213, no. 3 (2017): 261–266.

[451]

T. Mashima, S. Sato, Y. Sugimoto, T. Tsuruo, and H. Seimiya, “Promotion of Glioma Cell Survival by Acyl-CoA Synthetase 5 Under Extracellular Acidosis Conditions,” Oncogene 28, no. 1 (2009): 9–19.

[452]

Y. Di, Z. Wang, J. Xiao, et al., “ACSL6-activated IL-18R1-NF-κB Promotes IL-18-mediated Tumor Immune Evasion and Tumor Progression,” Science Advances 10, no. 38 (2024): eadp0719.

[453]

H. Hua, S. Pan, H. Diao, Y. Cao, X. Qian, and J. Zhang, “Increased ACSL6 Expression Predicts a Favorable Prognosis in Triple-negative Breast Cancer,” Current Medicinal Chemistry (2024), Published online January 17.

[454]

Y. Tang, W. Tian, J. Xie, et al., “Prognosis and Dissection of Immunosuppressive Microenvironment in Breast Cancer Based on Fatty Acid Metabolism-Related Signature,” Frontiers in Immunology 13 (2022): 843515.

[455]

Z. Jia, Z. Fu, Y. Kong, et al., “Fatty Acid Metabolism-related Genes as a Novel Module Biomarker for Kidney Renal Clear Cell Carcinoma: Bioinformatics Modeling With Experimental Verification,” Translational Oncology 38 (2023): 101774.

[456]

X. Chen, Z. Zhang, W. Liao, and Y. Zhao, “Assessment Tool Based on Fatty Acid Metabolic Signatures for Predicting the Prognosis and Treatment Response in Bladder Cancer,” Heliyon 9, no. 12 (2023): e22768.

[457]

C. Ye, Q. Sun, J. Yan, et al., “Development of Fatty Acid Metabolism Score Based on Gene Signature for Predicting Prognosis and Immunotherapy Response in Colon Cancer,” Clinical & Translational Oncology: official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico 26, no. 3 (2024): 630–643.

[458]

X. Huang, Y. Sun, J. Song, et al., “Prognostic Value of Fatty Acid Metabolism-related Genes in Colorectal Cancer and Their Potential Implications for Immunotherapy,” Frontiers in immunology 14 (2023): 1301452.

[459]

Y. Lin, R. Li, T. Li, et al., “A Prognostic Model for Hepatocellular Carcinoma Patients Based on Polyunsaturated Fatty Acid-related Genes,” Environmental Toxicology 39, no. 10 (2024): 4649–4668.

[460]

Y. Dong, K. Zhang, J. Wei, et al., “Gut Microbiota-derived Short-chain Fatty Acids Regulate Gastrointestinal Tumor Immunity: A Novel Therapeutic Strategy?” Frontiers in immunology 14 (2023): 1158200.

[461]

M. A. Feitelson, A. Arzumanyan, A. Medhat, and I. Spector, “Short-chain Fatty Acids in Cancer Pathogenesis,” Cancer and Metastasis Reviews 42, no. 3 (2023): 677–698.

[462]

S. Li, Y. Duan, S. Luo, F. Zhou, Q. Wu, and Z. Lu, “Short-chain fatty acids and cancer,” Trends in Cancer S2405-8033, no. 24 (2024): 00255–00253, Published online December 4.

[463]

M. Nomura, R. Nagatomo, K. Doi, et al., “Association of Short-Chain Fatty Acids in the Gut Microbiome with Clinical Response to Treatment with Nivolumab or Pembrolizumab in Patients with Solid Cancer Tumors,” JAMA Network Open 3, no. 4 (2020): e202895.

[464]

F. Hersi, S. M. Elgendy, S. A. Al Shamma, R. T. Altell, O. Sadiek, and H. A. Omar, “Cancer Immunotherapy Resistance: The Impact of Microbiome-derived Short-chain Fatty Acids and Other Emerging Metabolites,” Life Sciences 300 (2022): 120573.

[465]

X. Bi, J. Wang, and C. Liu, “Intratumoral Microbiota: Metabolic Influences and Biomarker Potential in Gastrointestinal Cancer,” Biomolecules 14, no. 8 (2024): 917.

[466]

A. Moratiel-Pellitero, M. Zapata-García, M. Gascón-Ruiz, et al., “Biomarkers of Immunotherapy Response in Patients With Non-Small-Cell Lung Cancer: Microbiota Composition, Short-Chain Fatty Acids, and Intestinal Permeability,” Cancers 16, no. 6 (2024): 1144.

[467]

B. Li, Y. Li, H. Zhou, et al., “Multiomics Identifies Metabolic Subtypes Based on Fatty Acid Degradation Allocating Personalized Treatment in Hepatocellular Carcinoma,” Hepatol Baltim Md 79, no. 2 (2024): 289–306.

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