Review Article

Mitochondria homeostasis: Biology and involvement in hepatic steatosis to NASH

Yu-feng Li1, Zhi-fu Xie1, Qian Song1,2, Jing-ya Li1,2,3
1 Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai 201203, China
2 University of Chinese Academy of Sciences, Beijing 100049, China
3 Hangzhou Institute for Advanced Study, University of Chinese Academy of Sciences, Hangzhou 310024, China
Correspondence to: Jing-ya Li:,
DOI: 10.1038/s41401-022-00864-z
Received: 15 November 2021
Accepted: 9 January 2022
Advance online: 1 February 2022


Mitochondrial biology and behavior are central to the physiology of liver. Multiple mitochondrial quality control mechanisms remodel mitochondrial homeostasis under physiological and pathological conditions. Mitochondrial dysfunction and damage induced by overnutrition lead to oxidative stress, inflammation, liver cell death, and collagen production, which advance hepatic steatosis to nonalcoholic steatohepatitis (NASH). Accumulating evidence suggests that specific interventions that target mitochondrial homeostasis, including energy metabolism, antioxidant effects, and mitochondrial quality control, have emerged as promising strategies for NASH treatment. However, clinical translation of these findings is challenging due to the complex and unclear mechanisms of mitochondrial homeostasis in the pathophysiology of NASH.
Keywords: liver; NASH; mitochondria; metabolism; mitochondrial homeostasis

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