Ferroptosis in Osteoarthritis: Towards Novel Therapeutic Strategy

Yiming Zhang , Jing Li , Jiane Liu , Yan Gao , Kehan Li , Xinyu Zhao , Yufeng Liu , Daijie Wang , Xiao Hu , Zheng Wang

Cell Proliferation ›› 2025, Vol. 58 ›› Issue (3) : e13779

PDF
Cell Proliferation ›› 2025, Vol. 58 ›› Issue (3) : e13779 DOI: 10.1111/cpr.13779
REVIEW

Ferroptosis in Osteoarthritis: Towards Novel Therapeutic Strategy

Author information +
History +
PDF

Abstract

Osteoarthritis (OA) is a chronic, degenerative joint disease primarily characterised by damage to the articular cartilage, synovitis and persistent pain, and has become one of the most common diseases worldwide. In OA cartilage, various forms of cell death have been identified, including apoptosis, necroptosis and autophagic cell death. Ever-growing observations indicate that ferroptosis, a newly-discovered iron-dependent form of regulated cell death, is detrimental to OA occurrence and progression. In this review, we first analyse the pathogenetic mechanisms of OA by which iron overload, inflammatory response and mechanical stress contribute to ferroptosis. We then discuss how ferroptosis exacerbates OA progression, focusing on its impact on chondrocyte viability, synoviocyte populations and extracellular matrix integrity. Finally, we highlight several potential therapeutic strategies targeting ferroptosis that could be explored for the treatment of OA.

Keywords

ferroptosis / mechanism / osteoarthritis / therapeutic strategy

Cite this article

Download citation ▾
Yiming Zhang, Jing Li, Jiane Liu, Yan Gao, Kehan Li, Xinyu Zhao, Yufeng Liu, Daijie Wang, Xiao Hu, Zheng Wang. Ferroptosis in Osteoarthritis: Towards Novel Therapeutic Strategy. Cell Proliferation, 2025, 58(3): e13779 DOI:10.1111/cpr.13779

登录浏览全文

4963

注册一个新账户 忘记密码

References

[1]

D. J. Hunter, L. March, and M. Chew, “Osteoarthritis in 2020 and Beyond: a Lancet Commission,” Lancet 396, no. 10264 (2020): 1711-1712.

[2]

L. Yue and J. Berman, “What Is Osteoarthritis?,” Journal of the American Medical Association 327, no. 13 (2022): 1300.

[3]

I. Morales-Ivorra, M. Romera-Baures, B. Roman-Viñas, and L. Serra-Majem, “Osteoarthritis and the Mediterranean Diet: A Systematic Review,” Nutrients 10, no. 8 (2018): 1030-1040.

[4]

Y. Hattori, K. Doi, B. Dormitorio, and S. Sakamoto, “Arthrodesis for Primary Osteoarthritis of the Trapeziometacarpal Joint in Elderly Patients,” Journal of Hand Surgery 41, no. 7 (2016): 753-759.

[5]

J. Harlaar, E. M. Macri, and M. Wesseling, “Osteoarthritis Year in Review 2021: Mechanics,” Osteoarthritis and Cartilage 30, no. 5 (2022): 663-670.

[6]

R. Zhu, Y. Wang, Z. Ouyang, et al., “Targeting Regulated Chondrocyte Death in Osteoarthritis Therapy,” Biochemical Pharmacology 215 (2023): 115707.

[7]

B. Wang, Y. Wang, J. Zhang, et al., “ROS-Induced Lipid Peroxidation Modulates Cell Death Outcome: Mechanisms Behind Apoptosis, Autophagy, and Ferroptosis,” Archives of Toxicology 97 (2023): 1439-1451.

[8]

S. J. Dixon, K. M. Lemberg, M. R. Lamprecht, et al., “Ferroptosis: An Iron-Dependent Form of Nonapoptotic Cell Death,” Cell 149, no. 5 (2012): 1060-1072.

[9]

S. Wang, X. He, Q. Wu, et al., “Transferrin Receptor 1-Mediated Iron Uptake Plays an Essential Role in Hematopoiesis,” Haematologica 105, no. 8 (2020): 2071-2082.

[10]

A. Kalemos, “Fe2: As Simple as a Herculean Labour. Neutral (Fe2), Cationic (Fe2(+)), and Anionic (Fe2(−)) Species,” Journal of Chemical Physics 142, no. 24 (2015): 244304.

[11]

N. A. Wolff, A. J. Ghio, L. M. Garrick, et al., “Evidence for Mitochondrial Localization of Divalent Metal Transporter 1 (DMT1),” FASEB Journal 28, no. 5 (2014): 2134-2145.

[12]

A. Treffry, P. M. Harrison, M. I. Cleton, W. C. de Bruijn, and S. Mann, “A Note on the Composition and Properties of Ferritin Iron Cores,” Journal of Inorganic Biochemistry 31, no. 1 (1987): 1-6.

[13]

M. Gryzik, A. Srivastava, G. Longhi, et al., “Expression and Characterization of the Ferritin Binding Domain of Nuclear Receptor Coactivator-4 (NCOA4),” Biochimica et Biophysica Acta (BBA) - General Subjects 1861, no. 11 (2017): 2710-2716.

[14]

J. F. Ying, Z. B. Lu, L. Q. Fu, et al., “The Role of Iron Homeostasis and Iron-Mediated ROS in Cancer,” American Journal of Cancer Research 11, no. 5 (2021): 1895-1912.

[15]

A. Ayala, M. F. Muñoz, and S. Argüelles, “Lipid peroxidation: Production, Metabolism, and Signaling Mechanisms of Malondialdehyde and 4-Hydroxy-2-Nonenal,” Oxidative Medicine and Cellular Longevity 2014 (2014): 360438.

[16]

F. Zhang, Y. Yan, Y. Cai, et al., “Current Insights Into the Functional Roles of Ferroptosis in Musculoskeletal Diseases and Therapeutic Implications,” Frontiers in Cell and Developmental Biology 11 (2023): 1112751.

[17]

J. Lewerenz, S. J. Hewett, Y. Huang, et al., “The Cystine/Glutamate Antiporter System x(c)(−) in Health and Disease: From Molecular Mechanisms to Novel Therapeutic Opportunities,” Antioxidants & Redox Signaling 18, no. 5 (2013): 522-555.

[18]

Y. Zhang, R. V. Swanda, L. Nie, et al., “mTORC1 Couples Cyst(e)ine Availability With GPX4 Protein Synthesis and Ferroptosis Regulation,” Nature Communications 12, no. 1 (2021): 1589.

[19]

S. Doll, F. P. Freitas, R. Shah, et al., “FSP1 is a Glutathione-Independent Ferroptosis Suppressor,” Nature 575, no. 7784 (2019): 693-698.

[20]

J. Zheng and M. Conrad, “The Metabolic Underpinnings of Ferroptosis,” Cell Metabolism 32, no. 6 (2020): 920-937.

[21]

H. Fanet, L. Capuron, N. Castanon, F. Calon, and S. Vancassel, “Tetrahydrobioterin (BH4) Pathway: From Metabolism to Neuropsychiatry,” Current Neuropharmacology 19, no. 5 (2021): 591-609.

[22]

J. Chen, Y. Wang, J. Wu, J. Yang, M. Li, and Q. Chen, “The Potential Value of Targeting Ferroptosis in Early Brain Injury After Acute CNS Disease,” Frontiers in Molecular Neuroscience 13 (2020): 110.

[23]

C. Guo, J. Peng, P. Cheng, et al., “Mechanistic Elucidation of Ferroptosis and Ferritinophagy: Implications for Advancing Our Understanding of Arthritis,” Frontiers in Physiology 15 (2024): 1290234.

[24]

S. Milic, I. Mikolasevic, L. Orlic, et al., “The Role of Iron and Iron Overload in Chronic Liver Disease,” Medical Science Monitor: International Medical Journal of Experimental and Clinical Research 22 (2016): 2144-2151.

[25]

T. Meroño, L. Gómez Rosso, P. Sorroche, L. Boero, J. Arbelbide, and F. Brites, “High Risk of Cardiovascular Disease in Iron Overload Patients,” European Journal of Clinical Investigation 41, no. 5 (2011): 479-486.

[26]

A. V. Harrison, F. R. Lorenzo, and D. A. McClain, “Iron and the Pathophysiology of Diabetes,” Annual Review of Physiology 85 (2023): 339-362.

[27]

R. J. Ward, F. A. Zucca, J. H. Duyn, R. R. Crichton, and L. Zecca, “The Role of Iron in Brain Ageing and Neurodegenerative Disorders,” Lancet Neurology 13, no. 10 (2014): 1045-1060.

[28]

V. Jeney, “Clinical Impact and Cellular Mechanisms of Iron Overload-Associated Bone Loss,” Frontiers in Pharmacology 8 (2017): 77.

[29]

L. H. Burton, M. F. Afzali, L. B. Radakovich, et al., “Systemic Administration of a Pharmacologic Iron Chelator Reduces Cartilage Lesion Development in the Dunkin-Hartley Model of Primary Osteoarthritis,” Free Radical Biology and Medicine 179 (2022): 47-58.

[30]

L. Wu, H. Si, Y. Zeng, et al., “Association Between Iron Intake and Progression of Knee Osteoarthritis,” Nutrients 14, no. 8 (2022): 1674-1684.

[31]

M. Yazar, S. Sarban, A. Kocyigit, and U. E. Isikan, “Synovial Fluid and Plasma Selenium, Copper, Zinc, and Iron Concentrations in Patients With Rheumatoid Arthritis and Osteoarthritis,” Biological Trace Element Research 106, no. 2 (2005): 123-132.

[32]

Y. Sun, B. P. Scannell, P. R. Honeycutt, D. R. Mauerhan, J. N. H, and E. N. Hanley, “Cartilage Degeneration, Subchondral Mineral and Meniscal Mineral Densities in Hartley and Strain 13 Guinea Pigs,” Open Rheumatology Journal 9 (2015): 65-70.

[33]

X. Zhang, L. Hou, Z. Guo, et al., “Lipid Peroxidation in Osteoarthritis: Focusing on 4-Hydroxynonenal, Malondialdehyde, and Ferroptosis,” Cell Death Discovery 9, no. 1 (2023): 320.

[34]

C. Reyes, K. M. Leyland, G. Peat, C. Cooper, N. K. Arden, and D. Prieto-Alhambra, “Association Between Overweight and Obesity and Risk of Clinically Diagnosed Knee, Hip, and Hand Osteoarthritis: A Population-Based Cohort Study,” Arthritis and Rheumatology 68, no. 8 (2016): 1869-1875.

[35]

R. C. Koonce and J. T. Bravman, “Obesity and Osteoarthritis: More Than Just Wear and Tear,” American Academy of Orthopaedic Surgeon 21, no. 3 (2013): 161-169.

[36]

P. F. Argote, J. T. Kaplan, A. Poon, et al., “Chondrocyte Viability is Lost During High-Rate Impact Loading by Transfer of Amplified Strain, but Not Stress, to Pericellular and Cellular Regions,” Osteoarthritis and Cartilage 27, no. 12 (2019): 1822-1830.

[37]

S. Wang, W. Li, P. Zhang, et al., “Mechanical Overloading Induces GPX4-Regulated Chondrocyte Ferroptosis in Osteoarthritis via Piezo1 Channel Facilitated Calcium Influx,” Journal of Advanced Research 41 (2022): 63-75.

[38]

H. Liu, Z. Deng, B. Yu, et al., “Identification of SLC3A2 as a Potential Therapeutic Target of Osteoarthritis Involved in Ferroptosis by Integrating Bioinformatics, Clinical Factors and Experiments,” Cells 11, no. 21 (2022): 3430-3446.

[39]

W. Guo, K. Li, B. Sun, et al., “Dysregulated Glutamate Transporter SLC1A1 Propels Cystine Uptake via Xc(−) for Glutathione Synthesis in Lung Cancer,” Cancer Research 81, no. 3 (2021): 552-566.

[40]

S. J. Dixon, D. N. Patel, M. Welsch, et al., “Pharmacological Inhibition of Cystine-Glutamate Exchange Induces Endoplasmic Reticulum Stress and Ferroptosis,” eLife 3 (2014): e02523.

[41]

P. Wojdasiewicz, A. Poniatowski, and D. Szukiewicz, “The role of Inflammatory and Anti-Inflammatory Cytokines in the Pathogenesis of Osteoarthritis,” Mediators of Inflammation 2014 (2014): 561459.

[42]

T. Wang and C. He, “Pro-Inflammatory Cytokines: The Link Between Obesity and Osteoarthritis,” Cytokine & Growth Factor Reviews 44 (2018): 38-50.

[43]

T. Mabey and S. Honsawek, “Cytokines as Biochemical Markers for Knee Osteoarthritis,” World Journal of Orthopedics 6, no. 1 (2015): 95-105.

[44]

S. Zuo, W. Zou, R. M. Wu, et al., “Icariin Alleviates IL-1β-Induced Matrix Degradation By Activating The Nrf2/ARE Pathway In Human Chondrocytes,” Drug Design, Development and Therapy 13 (2019): 3949-3961.

[45]

X. Yao, K. Sun, S. Yu, et al., “Chondrocyte Ferroptosis Contribute to the Progression of Osteoarthritis,” Journal of Orthopaedic Translation 27 (2021): 33-43.

[46]

J. T. Rogers, “Ferritin Translation by Interleukin-1and Interleukin-6: the Role of Sequences Upstream of the Start Codons of the Heavy and Light Subunit Genes,” Blood 87, no. 6 (1996): 2525-2537.

[47]

K. Sun, L. Hou, Z. Guo, et al., “JNK-JUN-NCOA4 Axis Contributes to Chondrocyte Ferroptosis and Aggravates Osteoarthritis via Ferritinophagy,” Free Radical Biology and Medicine 200 (2023): 87-101.

[48]

H. Luo and R. Zhang, “Icariin Enhances Cell Survival in Lipopolysaccharide-Induced Synoviocytes by Suppressing Ferroptosis via the Xc-/GPX4 Axis,” Experimental and Therapeutic Medicine 21, no. 1 (2021): 72.

[49]

J. D. Mancias, X. Wang, S. P. Gygi, J. W. Harper, and A. C. Kimmelman, “Quantitative Proteomics Identifies NCOA4 as the Cargo Receptor Mediating Ferritinophagy,” Nature 509, no. 7498 (2014): 105-109.

[50]

L. Xia and N. Gong, “Identification and Verification of Ferroptosis-Related Genes in the Synovial Tissue of Osteoarthritis Using Bioinformatics Analysis,” Frontiers in Molecular Biosciences 9 (2022): 992044.

[51]

Y. Miao, Y. Chen, F. Xue, et al., “Contribution of Ferroptosis and GPX4's Dual Functions to Osteoarthritis Progression,” eBioMedicine 76 (2022): 103847.

[52]

S. Liang, Z. T. Lv, J. M. Zhang, et al., “Necrostatin-1 Attenuates Trauma-Induced Mouse Osteoarthritis and IL-1β Induced Apoptosis via HMGB1/TLR4/SDF-1 in Primary Mouse Chondrocytes,” Frontiers of Pharmacology 9 (2018): 1378.

[53]

W. Xu, B. Zhang, C. Xi, et al., “Ferroptosis Plays a Role in Human Chondrocyte of Osteoarthritis Induced by IL-1β In Vitro,” Cartilage 14 (2023): 466.

[54]

Z. Feng, F. Meng, F. Huo, et al., “Inhibition of Ferroptosis Rescues M2 Macrophages and Alleviates Arthritis by Suppressing the HMGB1/TLR4/STAT3 Axis in M1 Macrophages,” Redox Biology 75 (2024): 103255.

[55]

Z. Hu, L. Chen, J. Zhao, et al., “Lipoxin A(4) Ameliorates Knee Osteoarthritis Progression in Rats by Antagonizing Ferroptosis Through Activation of the ESR2/LPAR3/Nrf2 Axis in Synovial Fibroblast-Like Synoviocytes,” Redox Biology 73 (2024): 103143.

[56]

Q. Wu, D. Li, C. Huang, et al., “Glucose Control Independent Mechanisms Involved in the Cardiovascular Benefits of Glucagon-Like Peptide-1 Receptor Agonists,” Biomedicine & Pharmacotherapy 153 (2022): 113517.

[57]

A. Latourte, C. Cherifi, J. Maillet, et al., “Systemic Inhibition of IL-6/Stat3 Signalling Protects Against Experimental Osteoarthritis,” Annals of the Rheumatic Diseases 76, no. 4 (2017): 748-755.

[58]

K. Bersuker, J. M. Hendricks, Z. Li, et al., “The CoQ Oxidoreductase FSP1 Acts Parallel to GPX4 to Inhibit Ferroptosis,” Nature 575, no. 7784 (2019): 688-692.

[59]

R. M. Guerra and D. J. Pagliarini, “Coenzyme Q Biochemistry and Biosynthesis,” Trends in Biochemical Sciences 48, no. 5 (2023): 463-476.

[60]

X. Li, Y. Guo, S. Huang, et al., “Coenzyme Q10 Prevents the Interleukin-1 Beta Induced Inflammatory Response via Inhibition of MAPK Signaling Pathways in Rat Articular Chondrocytes,” Drug Development Research 78, no. 8 (2017): 403-410.

[61]

J. Lee, Y. S. Hong, J. H. Jeong, et al., “Coenzyme Q10 Ameliorates Pain and Cartilage Degradation in a Rat Model of Osteoarthritis by Regulating Nitric Oxide and Inflammatory Cytokines,” PLoS One 8, no. 7 (2013): e69362.

[62]

M. Liu, X. Y. Kong, Y. Yao, et al., “The Critical Role and Molecular Mechanisms of Ferroptosis in Antioxidant Systems: a Narrative Review,” Annals of Translational Medicine 10, no. 6 (2022): 368.

[63]

X. A. Zhang and H. Kong, “Mechanism of HIFs in Osteoarthritis,” Frontiers of Immunology 14 (2023): 1168799.

[64]

Z. Lin, J. Miao, T. Zhang, et al., “d-Mannose Suppresses Osteoarthritis Development In Vivo and Delays IL-1β-Induced Degeneration In Vitro by Enhancing Autophagy Activated via the AMPK Pathway,” Biomedicine & Pharmacotherapy 135 (2021): 111199.

[65]

X. Zhou, Y. Zheng, W. Sun, et al., “D-Mannose Alleviates Osteoarthritis Progression by Inhibiting Chondrocyte Ferroptosis in a HIF-2α-Dependent Manner,” Cell Proliferation 54, no. 11 (2021): e13134.

[66]

S. Yang, J. Kim, J. H. Ryu, et al., “Hypoxia-Inducible Factor-2alpha is a Catabolic Regulator of Osteoarthritic Cartilage Destruction,” Nature Medicine 16, no. 6 (2010): 687-693.

[67]

T. Saito, A. Fukai, A. Mabuchi, et al., “Transcriptional Regulation of Endochondral Ossification by HIF-2alpha During Skeletal Growth and Osteoarthritis Development,” Nature Medicine 16, no. 6 (2010): 678-686.

[68]

R. H. Herman, “Mannose Metabolism,” American Journal of Clinical Nutrition 24, no. 4 (1971): 488-498.

[69]

V. Sharma, M. Ichikawa, and H. H. Freeze, “Mannose Metabolism: More Than Meets the Eye,” Biochemical and Biophysical Research Communications 453, no. 2 (2014): 220-228.

[70]

Y. L. Ai, W. J. Wang, F. J. Liu, et al., “Mannose Antagonizes GSDME-Mediated Pyroptosis Through AMPK Activated by Metabolite GlcNAc-6P,” Cell Research 33, no. 12 (2023): 904-922.

[71]

H. Lee, F. Zandkarimi, Y. Zhang, et al., “Energy-Stress-Mediated AMPK Activation Inhibits Ferroptosis,” Nature Cell Biology 22, no. 2 (2020): 225-234.

[72]

T. C. Huang, W. T. Chang, Y. C. Hu, et al., “Zinc Protects Articular Chondrocytes Through Changes in Nrf2-Mediated Antioxidants, Cytokines and Matrix Metalloproteinases,” Nutrients 10, no. 4 (2018): 471-486.

[73]

L. Rochette, G. Dogon, E. Rigal, M. Zeller, Y. Cottin, and C. Vergely, “Lipid Peroxidation and Iron Metabolism: Two Corner Stones in the Homeostasis Control of Ferroptosis,” International Journal of Molecular Sciences 24, no. 1 (2022): 449-467.

[74]

M. Dodson, R. Castro-Portuguez, and D. D. Zhang, “NRF2 Plays a Critical Role in Mitigating Lipid Peroxidation and Ferroptosis,” Redox Biology 23 (2019): 101107.

[75]

J. Zhou, C. Liu, Y. Sun, et al., “Genetically Predicted Circulating Levels of Copper and Zinc are Associated with Osteoarthritis but Not With Rheumatoid Arthritis,” Osteoarthritis and Cartilage 29, no. 7 (2021): 1029-1035.

[76]

J. H. Kim, J. Jeon, M. Shin, et al., “Regulation of the Catabolic Cascade in Osteoarthritis by the Zinc-ZIP8-MTF1 Axis,” Cell 156, no. 4 (2014): 730-743.

[77]

C. Vinatier, C. Merceron, and J. Guicheux, “Osteoarthritis: From Pathogenic Mechanisms and Recent Clinical Developments to Novel Prospective Therapeutic Options,” Drug Discovery Today 21, no. 12 (2016): 1932-1937.

[78]

I. Davan, S. Fakurazi, E. Alias, N. I. Ibrahim, N. M. Hwei, and H. Hassan, “Astaxanthin as a Potent Antioxidant for Promoting Bone Health: An Up-to-Date Review,” Antioxidants (Basel) 12, no. 7 (2023): 1480-1505.

[79]

G. Yang, X. Liu, X. Jing, et al., “Astaxanthin Suppresses Oxidative Stress and Calcification in Vertebral Cartilage Endplate via Activating Nrf-2/HO-1 Signaling Pathway,” International Immunopharmacology 119 (2023): 110159.

[80]

X. Wang, Z. Liu, P. Peng, Z. Gong, J. Huang, and H. Peng, “Astaxanthin Attenuates Osteoarthritis Progression via Inhibiting Ferroptosis and Regulating Mitochondrial Function in Chondrocytes,” Chemico-Biological Interactions 366 (2022): 110148.

[81]

C. Zhu, G. Liu, W. Cui, et al., “Astaxanthin Prevents Osteoarthritis by Blocking Rspo2-Mediated Wnt/β-Catenin Signaling in Chondrocytes and Abolishing Rspo2-Related Inflammatory Factors in Macrophages,” Aging (Albany NY) 15, no. 12 (2023): 5775-5797.

[82]

C. Q. Xu, B. J. Liu, J. F. Wu, et al., “Icariin Attenuates LPS-Induced Acute Inflammatory Responses: Involvement of PI3K/Akt and NF-kappaB Signaling Pathway,” European Journal of Pharmacology 642, no. 1-3 (2010): 146-153.

[83]

S. C. Sze, Y. Tong, T. B. Ng, et al., “Herba Epimedii: Anti-Oxidative Properties and its Medical Implications,” Molecules 15, no. 11 (2010): 7861-7870.

[84]

B. Zhang, G. Wang, J. He, et al., “Icariin Attenuates Neuroinflammation and Exerts Dopamine Neuroprotection via an Nrf2-Dependent Manner,” Journal of Neuroinflammation 16, no. 1 (2019): 92.

[85]

S. Kapoor, “Icariin and its Emerging Role in the Treatment of Osteoporosis,” Chinese Medical Journal 126, no. 2 (2013): 400.

[86]

P. Sithisarn, M. Michaelis, M. Schubert-Zsilavecz, and J. Cinatl, “Differential Antiviral and Anti-Inflammatory Mechanisms of the Flavonoids Biochanin A and Baicalein in H5N1 Influenza A Virus-Infected Cells,” Antiviral Research 97, no. 1 (2013): 41-48.

[87]

J. Wang, C. He, W. Y. Wu, et al., “Biochanin A Protects Dopaminergic Neurons Against Lipopolysaccharide-Induced Damage and Oxidative Stress in a Rat Model of Parkinson's Disease,” Pharmacology Biochemistry and Behavior 138 (2015): 96-103.

[88]

J. W. Tan and M. K. Kim, “Neuroprotective Effects of Biochanin A against β-Amyloid-Induced Neurotoxicity in PC12 Cells via a Mitochondrial-Dependent Apoptosis Pathway,” Molecules 21, no. 5 (2016): 548-561.

[89]

Q. He, J. Yang, Z. Pan, et al., “Biochanin A Protects Against Iron Overload Associated Knee Osteoarthritis via Regulating Iron Levels and NRF2/System xc-/GPX4 Axis,” Biomedicine & Pharmacotherpy 157 (2023): 113915.

[90]

C. Xu, S. Ni, N. Xu, et al., “Theaflavin-3,3'-Digallate Inhibits Erastin-Induced Chondrocytes Ferroptosis via the Nrf2/GPX4 Signaling Pathway in Osteoarthritis,” Oxidative Medicine and Cellular Longevity 2022 (2022): 3531995.

[91]

L. Wang, Y. Liu, T. du, et al., “ATF3 Promotes Erastin-Induced Ferroptosis by Suppressing System Xc(−),” Cell Death and Differentiation 27, no. 2 (2020): 662-675.

[92]

G. Mesquita, T. Silva, A. C. Gomes, et al., “H-Ferritin is Essential for Macrophages' Capacity to Store or Detoxify Exogenously Added Iron,” Scientific Reports 10, no. 1 (2020): 3061.

[93]

D. Kim, D. Lee, D. Oh, et al., “A Mixture Containing Fermented Achyranthes japonica Nakai Ameliorates Osteoarthritis in Knee Joints of Monoiodoacetate-Injected Rats,” Journal of Medicinal Food 23, no. 8 (2020): 811-817.

[94]

W. P. Chen, C. Yu, P. F. Hu, J. P. Bao, J. L. Tang, and L. D. Wu, “Stigmasterol Blocks Cartilage Degradation in Rabbit Model of Osteoarthritis,” Acta Biochimica Polonica 59, no. 4 (2012): 537-541.

[95]

Z. S. Mo, P. Q. Xu, and H. Y. Li, “Stigmasterol Alleviates Interleukin-1beta-Induced Chondrocyte Injury by Down-Regulatingsterol Regulatory Element Binding Transcription Factor 2 to Regulateferroptosis,” Bioengineered 12, no. 2 (2021): 9332-9340.

[96]

X. M. Qiu, C. T. Jin, and W. Wang, “Association Between Single Nucleotide Polymorphisms of Sterol Regulatory Element Binding Protein-2 Gene and Risk of Knee Osteoarthritis in a Chinese Han population,” Journal of International Medical Research 42, no. 2 (2014): 320-328.

[97]

F. Kostopoulou, V. Gkretsi, K. N. Malizos, et al., “Central Role of SREBP-2 in the Pathogenesis of Osteoarthritis,” PLoS One 7, no. 5 (2012): e35753.

[98]

X. Hong, W. Roh, R. J. Sullivan, et al., “The Lipogenic Regulator SREBP2 Induces Transferrin in Circulating Melanoma Cells and Suppresses Ferroptosis,” Cancer Discovery 11, no. 3 (2021): 678-695.

[99]

K. B. Barber, P. Mendonca, and K. F. A. Soliman, “The Neuroprotective Effects and Therapeutic Potential of the Chalcone Cardamonin for Alzheimer's Disease,” Brain Sciences 13, no. 1 (2023): 145-171.

[100]

Y. J. Peng, J. W. Lu, C. H. Lee, et al., “Cardamonin Attenuates Inflammation and Oxidative Stress in Interleukin-1β-Stimulated Osteoarthritis Chondrocyte through the Nrf2 Pathway,” Antioxidants (Basel) 10, no. 6 (2021): 862-878.

[101]

J. Jiang and M. Cai, “Cardamonin Inhibited IL-1β Induced Injury by Inhibition of NLRP3 Inflammasome via Activating Nrf2/NQO-1 Signaling Pathway in Chondrocyte,” Journal of Microbiology and Biotechnology 31, no. 6 (2021): 794-802.

[102]

Z. Gong, Y. Wang, L. Li, X. Li, B. Qiu, and Y. Hu, “Cardamonin Alleviates Chondrocytes Inflammation and Cartilage Degradation of Osteoarthritis by Inhibiting Ferroptosis via p53 Pathway,” Food and Chemical Toxicology 174 (2023): 113644.

[103]

C. C. Wang, J. W. Lu, Y. J. Peng, et al., “Ameliorative Effects of Cardamonin on Monosodium Urate-Induced Gouty Arthritis Through Inhibiting NLRP3 Inflammasome Mediation,” Medicina (Kaunas, Lithuania) 57, no. 9 (2021): 898-908.

[104]

S. Jaiswal, A. Sharma, M. Shukla, and J. Lal, “Gender-Related Pharmacokinetics and Bioavailability of a Novel Anticancer Chalcone, Cardamonin, in Rats Determined by Liquid Chromatography Tandem Mass Spectrometry,” Journal of Chromatography B 986 (2015): 23-30.

[105]

S. Jaiswal, M. Shukla, A. Sharma, et al., “Preclinical Pharmacokinetics and ADME Characterization of a Novel Anticancer Chalcone, Cardamonin,” Drug Testing and Analysis 9, no. 8 (2017): 1124-1136.

[106]

T. Ogura, B. A. Mosier, T. Bryant, and T. Minas, “A 20-Year Follow-up After First-Generation Autologous Chondrocyte Implantation,” American Journal of Sports Medicine 45, no. 12 (2017): 2751-2761.

[107]

D. Martinčič, J. Mekač, and M. Drobnič, “Survival Rates of Various Autologous Chondrocyte Grafts and Concomitant Procedures. A Prospective Single-Center Study Over 18 Years,” Cell Transplantation 28, no. 11 (2019): 1439-1444.

[108]

A. Tekari, R. Luginbuehl, W. Hofstetter, and R. J. Egli, “Chondrocytes Expressing Intracellular Collagen Type II Enter the Cell Cycle and Co-Express Collagen Type I in Monolayer Culture,” Journal of Orthopaedic Research 32, no. 11 (2014): 1503-1511.

[109]

M. E. Fernández-Santos, M. Garcia-Arranz, E. J. Andreu, et al., “Optimization of Mesenchymal Stromal Cell (MSC) Manufacturing Processes for a Better Therapeutic Outcome,” Frontiers of Immunology 13 (2022): 918565.

[110]

X. Zhu, X. Xu, M. Shen, et al., “Transcriptomic Heterogeneity of Human Mesenchymal Stem Cells Derived from Bone Marrow, Dental Pulp, Adipose Tissue, and Umbilical Cord,” Cellular Reprogramming 25, no. 4 (2023): 162-170.

[111]

F. Djouad, C. Bouffi, S. Ghannam, D. Noël, and C. Jorgensen, “Mesenchymal Stem Cells: Innovative Therapeutic Tools for Rheumatic Diseases,” Nature Reviews Rheumatology 5, no. 7 (2009): 392-399.

[112]

S. Huang, X. Song, T. Li, et al., “Pellet Coculture of Osteoarthritic Chondrocytes and Infrapatellar Fat Pad-Derived Mesenchymal Stem Cells With Chitosan/Hyaluronic Acid Nanoparticles Promotes Chondrogenic Differentiation,” Stem Cell Research & Therapy 8, no. 1 (2017): 264.

[113]

A. Singh, S. C. Goel, K. K. Gupta, et al., “The Role of Stem Cells in Osteoarthritis: An Experimental Study in Rabbits,” Bone & Joint Research 3, no. 2 (2014): 32-37.

[114]

S. Peng, C. Sun, C. Lai, and L. Zhang, “Exosomes Derived From Mesenchymal Stem Cells Rescue Cartilage Injury in Osteoarthritis Through Ferroptosis by GOT1/CCR2 Expression,” International Immunopharmacology 122 (2023): 110566.

[115]

S. Cheng, X. Xu, R. Wang, W. Chen, K. Qin, and J. Yan, “Chondroprotective Effects of Bone Marrow Mesenchymal Stem Cell-Derived Exosomes in Osteoarthritis,” Journal of Bioenergetics and Biomembranes 56, no. 1 (2024): 31-44.

[116]

B. Chen, J. Yu, Q. Wang, et al., “c-MycHuman Bone Marrow Mesenchymal Stem Cells Promote Gastric Cancer Growth via Regulating,” Stem Cells International 2018, no. 1 (2018): 9501747.

[117]

Y. Zhao, Y. Wang, Z. Miao, Y. Liu, and Q. Yang, “c-Myc Protects Hepatocellular Carcinoma Cell From Ferroptosis Induced by Glutamine Deprivation via Upregulating GOT1 and Nrf2,” Molecular Biology Reports 50, no. 8 (2023): 6627-6641.

[118]

M. Icriverzi, V. Dinca, M. Moisei, R. W. Evans, M. Trif, and A. Roseanu, “Lactoferrin in Bone Tissue Regeneration,” Current Medicinal Chemistry 27, no. 6 (2020): 838-853.

[119]

H. M. Habib, S. Ibrahim, A. Zaim, and W. H. Ibrahim, “The Role of Iron in the Pathogenesis of COVID-19 and Possible Treatment With Lactoferrin and Other Iron Chelators,” Biomedicine & Pharmacotherpy 136 (2021): 111228.

[120]

X. Shan, J. Li, J. Liu, et al., “Targeting Ferroptosis by Poly(acrylic) Acid Coated Mn(3)O(4) Nanoparticles Alleviates Acute Liver Injury,” Nature Communications 14, no. 1 (2023): 7598.

[121]

X. Zhao, Z. Wang, G. Wu, et al., “Apigenin-7-Glucoside-Loaded Nanoparticle Alleviates Intestinal Ischemia-Reperfusion by ATF3/SLC7A11-Mediated Ferroptosis,” Journal of Controlled Release 366 (2024): 182-193.

[122]

R. Karki, B. R. Sharma, S. Tuladhar, et al., “Synergism of TNF-α and IFN-γ Triggers Inflammatory Cell Death, Tissue Damage, and Mortality in SARS-CoV-2 Infection and Cytokine Shock Syndromes,” Cell 184, no. 1 (2021): 149-168.e17.

[123]

Y. Palacios, L. A. Ramón-Luing, A. Ruiz, et al., “COVID-19 Patients With High TNF/IFN-γ Levels Show Hallmarks of PANoptosis, an Inflammatory Cell Death,” Microbes and Infection 25, no. 8 (2023): 105179.

[124]

C. Shi, P. Cao, Y. Wang, et al., “PANoptosis: A Cell Death Characterized by Pyroptosis, Apoptosis, and Necroptosis,” Journal of Inflammation Research 16 (2023): 1523-1532.

[125]

L. Galluzzi, I. Vitale, S. A. Aaronson, et al., “Molecular Mechanisms of Cell Death: Recommendations of the Nomenclature Committee on Cell Death 2018,” Cell Death and Differentiation 25, no. 3 (2018): 486-541.

[126]

Y. E. Henrotin, P. Bruckner, and J. P. Pujol, “The Role of Reactive Oxygen Species in Homeostasis and Degradation of Cartilage,” Osteoarthritis and Cartilage 11, no. 10 (2003): 747-755.

[127]

M. Y. Ansari, N. Ahmad, and T. M. Haqqi, “Oxidative stress and inflammation in osteoarthritis pathogenesis: Role of polyphenols,” Biomedicine & Pharmacotherapy 129 (2020): 110452.

[128]

L. Liu, P. Luo, M. Yang, J. Wang, W. Hou, and P. Xu, “The Role of Oxidative Stress in the Development of Knee Osteoarthritis: A Comprehensive Research Review,” Frontiers in Molecular Biosciences 9 (2022): 1001212.

[129]

B. Li, K. Cheng, T. Wang, et al., “Research Progress on GPX4 Targeted Compounds,” European Journal of Medicinal Chemistry 274 (2024): 116548.

[130]

L. Liu, Y. Ye, R. Lin, et al., “Ferroptosis: A Promising Candidate for Exosome-Mediated Regulation in Different Diseases,” Cell Communication and Signaling 22, no. 1 (2024): 6.

[131]

Z. Long, Y. Luo, M. Yu, X. Wang, L. Zeng, and K. Yang, “Targeting Ferroptosis: a New Therapeutic Opportunity for Kidney Diseases,” Frontiers of Immunology 15 (2024): 1435139.

[132]

Y. Su, N. Cao, D. Zhang, and M. Wang, “The Effect of Ferroptosis-Related Mitochondrial Dysfunction in the Development of Temporal Lobe Epilepsy,” Ageing Research Reviews 96 (2024): 102248.

[133]

C. Peleman, S. Francque, and T. V. Berghe, “Emerging Role of Ferroptosis in Metabolic Dysfunction-Associated Steatotic Liver Disease: Revisiting Hepatic Lipid Peroxidation,” eBioMedicine 102 (2024): 105088.

[134]

J. Liu, R. Kang, and D. Tang, “Signaling pathways and defense mechanisms of ferroptosis,” FEBS Journal 289, no. 22 (2022): 7038-7050.

[135]

X. Gao, N. Guo, H. Xu, et al., “Ibuprofen Induces Ferroptosis of Glioblastoma Cells via Downregulation of Nuclear Factor Erythroid 2-Related Factor 2 Signaling Pathway,” Anti-Cancer Drugs 31, no. 1 (2020): 27-34.

[136]

Y. F. Wang, J. Y. Feng, L. N. Zhao, et al., “Aspirin Triggers Ferroptosis in Hepatocellular Carcinoma Cells Through Restricting NF-κB p65-Activated SLC7A11 Transcription,” Acta Pharmacologica Sinica 44, no. 8 (2023): 1712-1724.

[137]

W. Xie, Y. Lu, Y. Yuan, et al., “Hyaluronic Acid-Modified Spherical MgO(2)/Pd Nanocomposites Exhibit Superior Antitumor Effect through Tumor Microenvironment-Responsive Ferroptosis Induction and Photothermal Therapy,” ACS Biomaterials Science & Engineering 10, no. 8 (2024): 5226-5236.

[138]

Y. Li, M. Ma, X. Wang, et al., “Celecoxib Alleviates the DSS-Induced Ulcerative Colitis in Mice by Enhancing Intestinal Barrier Function, Inhibiting Ferroptosis and Suppressing Apoptosis,” Immunopharmacology and Immunotoxicology 46, no. 2 (2024): 240-254.

[139]

I. Golovach, D. Rekalov, O. Y. Akimov, et al., “Molecular Mechanisms and Potential Applications of Chondroitin Sulphate in Managing Post-Traumatic Osteoarthritis,” Reumatologia 61, no. 5 (2023): 395-407.

[140]

S. K. Ryan, C. L. Ugalde, A. S. Rolland, J. Skidmore, D. Devos, and T. R. Hammond, “Therapeutic Inhibition of Ferroptosis in Neurodegenerative Disease,” Trends in Pharmacological Sciences 44, no. 10 (2023): 674-688.

[141]

G. P. Neupane and D. M. Kim, “Comparison of the Effects of Deferasirox, Deferiprone, and Deferoxamine on the Growth and Virulence of Vibrio vulnificus,” Transfusion 49, no. 8 (2009): 1762-1769.

[142]

Z. Guo, J. Lin, K. Sun, et al., “Deferoxamine Alleviates Osteoarthritis by Inhibiting Chondrocyte Ferroptosis and Activating the Nrf2 Pathway,” Frontiers of Pharmacology 13 (2022): 791376.

[143]

H. Kuang, X. Sun, Y. Liu, et al., “Palmitic Acid-Induced Ferroptosis via CD36 Activates ER Stress to Break Calcium-Iron Balance in Colon Cancer Cells,” FEBS Journal 290, no. 14 (2023): 3664-3687.

[144]

W. Liu, Z. W. Tan, Y. C. Zhao, et al., “Panaxadiol Saponin Ameliorates Ferroptosis in Iron-Overload Aplastic Anemia Mice and Meg-01 Cells by Activating Nrf2/HO-1 and PI3K/AKT/mTOR Signaling Pathway,” International Immunopharmacology 118 (2023): 110131.

[145]

M. F. Beal, D. Oakes, I. Shoulson, et al., “A Randomized Clinical Trial of High-Dosage Coenzyme Q10 in Early Parkinson Disease: No Evidence of Benefit,” Journal of the American Medical Association Neurology 71, no. 5 (2014): 543-552.

[146]

C. Zhao, G. Sun, Y. Li, et al., “Forkhead Box O3 Attenuates Osteoarthritis by Suppressing Ferroptosis Through Inactivation of NF-κB/MAPK Signaling,” Journal of Orthopaedic Translation 39 (2023): 147-162.

[147]

W. He, X. Lin, and K. Chen, “Specificity Protein 1-Mediated ACSL4 Transcription Promoted the Osteoarthritis Progression Through Suppressing the Ferroptosis of Chondrocytes,” Journal of Orthopaedic Surgery and Research 18, no. 1 (2023): 188.

[148]

Z. Lv, J. Han, J. Li, et al., “Single cell RNA-Seq Analysis Identifies Ferroptotic Chondrocyte Cluster and Reveals TRPV1 as an Anti-Ferroptotic Target in Osteoarthritis,” eBioMedicine 84 (2022): 104258.

[149]

Q. Cheng, M. Chen, M. Liu, et al., “Semaphorin 5A Suppresses Ferroptosis Through Activation of PI3K-AKT-mTOR Signaling in Rheumatoid Arthritis,” Cell Death & Disease 13, no. 7 (2022): 608.

[150]

M. Lv, Y. Cai, W. Hou, et al., “The RNA-Binding Protein SND1 Promotes the Degradation of GPX4 by Destabilizing the HSPA5 mRNA and Suppressing HSPA5 Expression, Promoting Ferroptosis in Osteoarthritis Chondrocytes,” Inflammation Research 71, no. 4 (2022): 461-472.

[151]

M. Zhou, C. Zhai, K. Shen, et al., “miR-1 Inhibits the Ferroptosis of Chondrocyte by Targeting CX43 and Alleviates Osteoarthritis Progression,” Journal of Immunology Research 151 (2023): 2061071.

[152]

M. Brittberg, A. Lindahl, A. Nilsson, C. Ohlsson, O. Isaksson, and L. Peterson, “Treatment of Deep Cartilage Defects in the Knee With Autologous Chondrocyte Transplantation,” New England Journal of Medicine 331, no. 14 (1994): 889-895.

[153]

M. J. Bouma, M. van Iterson, B. Janssen, C. L. Mummery, D. C. F. Salvatori, and C. Freund, “Differentiation-Defective Human Induced Pluripotent Stem Cells Reveal Strengths and Limitations of the Teratoma Assay and In Vitro Pluripotency Assays,” Stem Cell Reports 8, no. 5 (2017): 1340-1353.

[154]

M. S. Lach, M. A. Rosochowicz, M. Richter, I. Jagiełło, W. M. Suchorska, and T. Trzeciak, “The Induced Pluripotent Stem Cells in Articular Cartilage Regeneration and Disease Modelling: Are We Ready for Their Clinical Use?,” Cells 11, no. 3 (2022): 529-555.

[155]

Y. Zhu, Y. Wang, B. Zhao, et al., “Comparison of Exosomes Secreted by Induced Pluripotent Stem Cell-Derived Mesenchymal Stem Cells and Synovial Membrane-Derived Mesenchymal Stem Cells for the Treatment of Osteoarthritis,” Stem Cell Research & Therapy 8, no. 1 (2017): 64.

[156]

M. Jeyaraman, B. Shivaraj, S. K. Bingi, R. Ranjan, S. Muthu, and M. Khanna, “Does Vehicle-Based Delivery of Mesenchymal Stromal Cells Give Superior Results in Knee Osteoarthritis? Meta-Analysis of Randomized Controlled Trials,” Journal of Clinical Orthopaedics and Trauma 25 (2022): 101772.

[157]

D. Zheng, Y. Dan, S. H. Yang, et al., “Controlled Chondrogenesis From Adipose-Derived Stem Cells by Recombinant Transforming Growth Factor-β3 Fusion Protein in Peptide Scaffolds,” Acta Biomaterialia 11 (2015): 191-203.

RIGHTS & PERMISSIONS

2024 The Author(s). Cell Proliferation published by Beijing Institute for Stem Cell and Regenerative Medicine and John Wiley & Sons Ltd.

AI Summary AI Mindmap
PDF

11

Accesses

0

Citation

Detail

Sections
Recommended

AI思维导图

/