自噬在非酒精性脂肪性肝病中的变化及作用

The change and function of autophagy in nonalcoholic fatty liver disease

自噬是一种溶酶体依赖性降解途径，已有大量研究报道，自噬参与了非酒精性脂肪性肝病（NAFLD）的发生及发展。在NAFLD早期，自噬增强，并可以通过抑制引起NAFLD的“二次打击”延缓NAFLD的进展。在NAFLD晚期，由于自噬相关基因（Atg）7降解、哺乳动物雷帕霉素靶蛋白通路过度激活、高胰岛素血症、自噬一溶酶体蛋白水解功能减弱、自噬体膜及溶酶体膜脂质构成改变、肝细胞内钙离子水平增加引起自噬减弱，加重了NAFLD。

Autophagy is a pathway of degradation dependent on lysosome. A number of studies reported autophagy was involved in the occurrence and development of nonalcoholic fatty liver disease （NAFLD）. Autophagy is enhanced in the early stage of NAFLD, and can delay the progress of NAFLD by inhibiting the ＂secondary stroke＂ which can induce NAFLD. In the late stage of NAFLD, degradation of autophagy related gene （Atg）7, activation of excessive mammalian rapamycin target protein pathway, hyperinsulinemia, dysfunction of autophagy-lysosome membrane protein hydrolysis, change of lipid composition in autophagnsome and lysosome membrane, increase of calcium in the hepatocyte can inhibit autophagy, thus aggravate NAFLD.