Unveiling the Crucial Nexus: Mitochondrial Quality Control as a Central Driver in Metabolic Dysfunction-Associated Steatotic Liver Disease Pathogenesis

Wenkai Fu; Junqi Wang; Nan Lu; Zhijiang Guo; Sang-Bing Ong; Yong Gao; Hao Zhou; Xing Chang; Miao Meng

doi:10.1111/cpr.70141

Cell Proliferation ›› 2026, Vol. 59 ›› Issue (2) :e70141 DOI: 10.1111/cpr.70141

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Unveiling the Crucial Nexus: Mitochondrial Quality Control as a Central Driver in Metabolic Dysfunction-Associated Steatotic Liver Disease Pathogenesis

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Wenkai Fu, Junqi Wang, Nan Lu, Zhijiang Guo, Sang-Bing Ong, Yong Gao, Hao Zhou, Xing Chang, Miao Meng. Unveiling the Crucial Nexus: Mitochondrial Quality Control as a Central Driver in Metabolic Dysfunction-Associated Steatotic Liver Disease Pathogenesis. Cell Proliferation, 2026, 59 (2) : e70141 DOI:10.1111/cpr.70141

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References

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[1]	T. Lv, X. Fan, C. He, et al., “SLC7A11-ROS/αKG-AMPK Axis Regulates Liver Inflammation Through Mitophagy and Impairs Liver Fibrosis and NASH Progression,” Redox Biology 72 (2024): 103159, https://doi.org/10.1016/j.redox.2024.103159.

[2]

K. A. Dias, L. A. Oliveira, S. M. S. Pereira, et al., “Anti-Inflammatory and Antioxidant Effects of Anthocyanins in Nonalcoholic Fatty Liver Disease (NAFLD): A Systematic Review of In Vivo Studies,” Critical Reviews in Food Science and Nutrition (2025): 1–18, https://doi.org/10.1080/10408398.2025.2472882.

[3]	Y. Chen, F. Yang, Y. Shi, et al., “RNF31 Alleviates Liver Steatosis by Promoting p53/BNIP3-Related Mitophagy in Hepatocytes,” Free Radical Biology & Medicine 219 (2024): 163–179, https://doi.org/10.1016/j.freeradbiomed.2024.04.214.

[4]

J. He, Y. C. Qian, Y. C. Yin, J. R. Kang, and T. R. Pan, “Polydatin: A Potential NAFLD Therapeutic Drug That Regulates Mitochondrial Autophagy Through SIRT3-FOXO3-BNIP3 and PINK1-PRKN Mechanisms: A Network Pharmacology and Experimental Investigation,” Chemico-Biological Interactions 398 (2024): 111110, https://doi.org/10.1016/j.cbi.2024.111110.

[5]	S. L. Xin, X. L. Pan, X. Y. Xu, and Y. Y. Yu, “USP10 Alleviates Palmitic Acid-Induced Steatosis Through Autophagy in HepG2 Cells,” Journal of Clinical and Translational Hepatology 11, no. 1 (2023): 45–57, https://doi.org/10.14218/JCTH.2022.00060.

[6]	W. Tong, L. Ju, M. Qiu, et al., “Liraglutide Ameliorates Non-Alcoholic Fatty Liver Disease by Enhancing Mitochondrial Architecture and Promoting Autophagy Through the SIRT1/SIRT3-FOXO3a Pathway,” Hepatology Research 46, no. 9 (2016): 933–943, https://doi.org/10.1111/hepr.12634.

[7]	M. Elbadawy, K. Tanabe, H. Yamamoto, et al., “Evaluation of the Efficacy of Mitochondrial Fission Inhibitor (Mdivi-1) Using Non-Alcoholic Steatohepatitis (NASH) Liver Organoids,” Frontiers in Pharmacology 14 (2023): 1243258, https://doi.org/10.3389/fphar.2023.1243258.

[8]

H. Li, Y. Jia, D. Yao, M. Gao, L. Wang, and J. Liu, “Rhein Alleviates Myocardial Ischemic Injury by Inhibiting Mitochondrial Division, Activating Mitochondrial Autophagy and Suppressing Myocardial Cell Apoptosis Through the Drp1/Pink1/Parkin Pathway,” Molecular Biology Reports 51, no. 1 (2024): 266, https://doi.org/10.1007/s11033-023-09154-1.

[9]	J. Liao, X. Xie, N. Wang, et al., “Formononetin Promotes Fatty Acid β-Oxidation to Treat Non-Alcoholic Steatohepatitis Through SIRT1/PGC-1α/PPARα Pathway,” Phytomedicine 124 (2024): 155285, https://doi.org/10.1016/j.phymed.2023.155285.

[10]	H. A. Hafez, A. M. Atoom, R. H. M. Khafaga, et al., “Direct-Acting Antiviral Drug Modulates the Mitochondrial Biogenesis in Different Tissues of Young Female Rats,” International Journal of Molecular Sciences 24, no. 21 (2023): 15844, https://doi.org/10.3390/ijms242115844.

[11]	S. A. Harrison, P. Bedossa, C. D. Guy, et al., “A Phase 3, Randomized, Controlled Trial of Resmetirom in NASH With Liver Fibrosis,” New England Journal of Medicine 390, no. 6 (2024): 497–509, https://doi.org/10.1056/NEJMoa2309000.

[12]	S. I. Yamashita, Y. Sugiura, Y. Matsuoka, et al., “Mitophagy Mediated by BNIP3 and NIX Protects Against Ferroptosis by Downregulating Mitochondrial Reactive Oxygen Species,” Cell Death and Differentiation 31, no. 5 (2024): 651–661, https://doi.org/10.1038/s41418-024-01280-y.

[13]	M. M. Syed-Abdul, “Lipid Metabolism in Metabolic-Associated Steatotic Liver Disease (MASLD),” Metabolites 14, no. 1 (2023): 12, https://doi.org/10.3390/metabo14010012.

[14]	C. He, Q. Zhang, R. Zhu, G. Tse, and W. T. Wong, “Asperuloside Activates Hepatic NRF2 Signaling to Stimulate Mitochondrial Metabolism and Restore Lipid Homeostasis in High Fat Diet-Induced MAFLD,” European Journal of Pharmacology 983 (2024): 177003, https://doi.org/10.1016/j.ejphar.2024.177003.

[15]	G. G. Lamanilao, M. Dogan, P. S. Patel, et al., “Key Hepatoprotective Roles of Mitochondria in Liver Regeneration,” American Journal of Physiology. Gastrointestinal and Liver Physiology 324, no. 3 (2023): G207–G218, https://doi.org/10.1152/ajpgi.00220.2022.

[16]	K. Cai, H. Jiang, Y. Zou, et al., “Programmed Death of Cardiomyocytes in Cardiovascular Disease and New Therapeutic Approaches,” Pharmacological Research 206 (2024): 107281, https://doi.org/10.1016/j.phrs.2024.107281.

[17]	G. Quarato, L. Mari, N. J. Barrows, et al., “Mitophagy Restricts BAX/BAK-Independent, Parkin-Mediated Apoptosis,” Science Advances 9, no. 21 (2023): eadg8156, https://doi.org/10.1126/sciadv.adg8156.

[18]	X. Pu, Q. Zhang, J. Liu, et al., “Ginsenoside Rb1 Ameliorates Heart Failure Through DUSP-1-TMBIM-6-Mediated Mitochondrial Quality Control and Gut Flora Interactions,” Phytomedicine 132 (2024): 155880, https://doi.org/10.1016/j.phymed.2024.155880.

[19]	J. Lin, H. Wang, R. Zhao, et al., “Ginsenoside re Ameliorates Thioacetamide-Induced Acute Liver Injury Through Inhibiting Autophagy-NLRP3 Inflammasome Pathway,” Frontiers in Pharmacology 16 (2025): 1592203, https://doi.org/10.3389/fphar.2025.1592203.

[20]	L. Tao, X. Yang, C. Ge, et al., “Integrative Clinical and Preclinical Studies Identify FerroTerminator1 as a Potent Therapeutic Drug for MASH,” Cell Metabolism 36, no. 10 (2024): 2190–2206.e5, https://doi.org/10.1016/j.cmet.2024.07.013.