自噬与氧化应激在非酒精性脂肪性肝病发病机制中的关系

Interrelation between autophagy and oxidative stress in pathogenesis of nonalcoholic fatty liver

非酒精性脂肪性肝病(NAFLD)是多种因素共同作用的结果,而以氧化应激为中心的"第二次打击"是NAFLD进展的关键因素。自噬作为近年来的研究热点,越来越多的证据显示自噬在肝细胞脂质代谢、炎症反应与肝纤维化中发挥重要作用,且与氧化应激有着密切关系。结合当前国内外最新研究成果分别从自噬与NAFLD的关系、氧化应激与NAFLD的关系分析自噬与氧化应激在NAFLD发病机制中的相互关系,指出自噬在NAFLD发病进程中调控氧化应激的分子机制可能成为今后的研究热点,若能够阻断或者激活自噬调控氧化应激的某个关键通路,或可为干预NAFLD提供新的手段。

Nonalcoholic fatty liver disease（ NAFLD） is the result of the interaction between many factors,and＂second hit＂focusing on oxidative stress is a key factor for the progression of NAFLD. Autophagy has been a research hotspot in recent years,and more and more studies have shown that autophagy plays an important role in lipid metabolism in hepatocytes,inflammatory response,and liver fibrosis and is closely associated with oxidative stress. With reference to the latest research findings in China and foreign countries,this article analyzes the interrelation between autophagy and oxidative stress in the pathogenesis of NAFLD from the aspects of the association between autophagy and NAFLD and the association between oxidative stress and NAFLD. It is pointed out that the molecular mechanism of the regulation of oxidative stress by autophagy in the pathogenesis of NAFLD may be a research hotspot in future,and blockade or activation of a key pathway involved in the regulation of oxidative stress by autophagy may provide a new method for the treatment of NAFLD.