Role of hepatocyte mitophagy in the pathogenesis of nonalcoholic fatty liver disease
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摘要: 非酒精性脂肪性肝病已成为我国第一大慢性肝病和健康体检肝生化指标异常的首要原因。线粒体自噬可降解肝脏中功能受损的线粒体和错误折叠蛋白以调节细胞死亡,同时具有维持肝脏脂质代谢稳态的作用。脂肪组织分泌的脂联素与脂联素受体2结合,可增加肝脏Kupffer细胞分泌自噬激动剂,诱导肝细胞线粒体自噬,促进脂质代谢,从而减轻肝脏炎症,为研发疗效显著和机制明确的非酒精性脂肪性肝病治疗药物提供了新思路。Abstract: Nonalcoholic fatty liver disease has become the most important chronic liver disease in China and the leading cause of abnormal liver biochemical parameters in physical examination. Mitophagy can degrade the mitochondria with impaired function and misfolded protein in the liver to regulate cell death and help to maintain stable lipid metabolism in the liver. The binding of adiponectin secreted by adipose tissue to adiponectin receptor 2 can increase the secretion of autophagy agonists in Kupffer cells,induce hepatocyte mitophagy,promote lipid metabolism,and thus reduce liver inflammation,which provides new thoughts for the research and development of drugs with a marked clinical effect and a clear mechanism of action in the treatment of nonalcoholic fatty liver disease.
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Key words:
- non-alcoholic fatty liver disease /
- adiponectin /
- mitochondria /
- autophagy
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