Abstract

Nonalcoholic steatohepatitis (NASH) is a common chronic liver disease characterized by hepatic steatosis, hepatocyte inflammation, and liver fibrosis. Studies have shown that mitochondrial disorders, such as abnormal lipid metabolism, reactive oxygen generation, damaged mitochondrial respiratory chain, mitochondrial rupture, and abnormal mitochondrial autophagy, play an important role in the development, progression, and prognosis of NASH. With the main clues of abnormal lipid metabolism, hepatitis, and liver fibrosis in NASH, this article reviews the mechanism of action of mitochondrial structural destruction, mitochondrial dysfunction, and impaired mitochondrial autophagy in NASH, so as to find corresponding targets for the treatment of NASH.

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