线粒体障碍在非酒精性脂肪性肝炎中的作用机制
DOI: 10.3969/j.issn.1001-5256.2021.08.045
利益冲突声明:所有作者均声明不存在利益冲突。
作者贡献声明:蔡恬莹负责课题设计,资料分析和撰写论文;黄美州、陈浩、钱保林参与收集数据,修改论文;付文广负责拟定写作思路,指导撰写文章并最后定稿。
Mechanism of action of mitochondrial disorders in nonalcoholic steatohepatitis
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摘要: 非酒精性脂肪性肝炎(NASH)是一种以肝脂肪变性、肝细胞炎症和肝纤维化为主要特征的常见慢性肝病。研究表明,线粒体内脂质代谢异常和活性氧生成、线粒体呼吸链受损、线粒体破裂以及线粒体自噬异常等线粒体障碍在NASH的发生、发展及转归过程中发挥重要作用。以NASH中肝脂肪代谢异常、肝炎发生和肝纤维化为主要线索,总结线粒体结构破坏、功能障碍以及线粒体自噬受损在NASH中的作用机制,以寻找相应靶点指导对NASH的治疗。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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Key words:
- Non-Alcoholic Fatty Liver Disease /
- Mitochondria /
- Autophagy
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