氧化应激与自噬在肝细胞癌发生发展中的作用

Role of oxidative stress and autophagy in the development and progression of hepatocellular carcinoma

肝细胞癌(HCC)是肝脏的原发恶性肿瘤,其发生过程十分复杂,氧化应激学说是其发生发展机制研究的众多重要学说之一。自噬是细胞清除胞内错误折叠的蛋白质或受损细胞器,维持内环境稳态的重要方式。越来越多的证据显示自噬在肝纤维化和HCC中发挥重要作用,且与氧化应激有密切关系。结合当前国内外最新研究成果,分别从自噬与HCC的关系、氧化应激与HCC的关系来分析二者在HCC发病机制中的相互作用。指出自噬在HCC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,若能够激活或阻断自噬调控氧化应激的某个关键通路,或可为HCC的早期诊断及治疗提供新的手段。

Hepatocellular carcinoma (HCC) is a primary malignant tumor of the liver and has a complex pathogenesis. At present, the oxidative stress theory is one of the many important theories for the mechanism of the development and progression of this disease. Autophagy is an important way for cells to clear misfolded proteins or damaged organelles and maintain homeostasis of the internal environment. An increasing number of evidence has shown that autophagy plays an important role in liver fibrosis and HCC and is closely associated with oxidative stress. With reference to the latest research findings around the world, this article analyzes the interaction between autophagy and oxidative stress in the pathogenesis of HCC from the aspect of their relationship with HCC. It is pointed out that the molecular mechanism by which autophagy regulates oxidative stress in the development of HCC may become a research hotspot in the future;it may provide a new means for the early diagnosis and treatment of HCC to activate or block a key pathway through which autophagy regulates oxidative stress.