Mitochondria homeostasis: Biology and involvement in hepatic steatosis to NASH

被引:23
作者
Li, Yu-feng [1 ]
Xie, Zhi-fu [1 ]
Song, Qian [1 ,2 ]
Li, Jing-ya [1 ,2 ,3 ]
机构
[1] Chinese Acad Sci, Shanghai Inst Mat Med, Shanghai 201203, Peoples R China
[2] Univ Chinese Acad Sci, Beijing 100049, Peoples R China
[3] Univ Chinese Acad Sci, Hangzhou Inst Adv Study, Hangzhou 310024, Peoples R China
基金
上海市自然科学基金; 中国博士后科学基金; 中国国家自然科学基金;
关键词
liver; NASH; mitochondria; metabolism; mitochondrial homeostasis; NONALCOHOLIC FATTY LIVER; ACTIVATED RECEPTOR-ALPHA; MESSENGER-RNA STABILITY; NLRP3 INFLAMMASOME ACTIVATION; OXIDATIVE STRESS; LIPID-METABOLISM; VITAMIN-E; SUCCINATE-DEHYDROGENASE; PROTEOLYTIC CLEAVAGE; ENERGY-METABOLISM;
D O I
10.1038/s41401-022-00864-z
中图分类号
O6 [化学];
学科分类号
0703 ;
摘要
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.
引用
收藏
页码:1141 / 1155
页数:15
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