细胞自噬与肝纤维化  

Autophagy and hepatic fibrosis

作　　者：钟佳[1] 杜瑶[1] 黄道斌[1] 杜芳腾[1] 张吉翔[1] 

机构地区：[1]南昌大学第二附属医院消化内科,南昌330006

出　　处：《生命的化学》2015年第1期15-18,共4页Chemistry of Life

基　　金：国家自然科学基金项目(30360037)

摘　　要：自噬是细胞内一种进化保守的依赖溶酶体的蛋白降解途径,存在于大多数真核细胞中,细胞自噬可以为应激状态(如炎症、肿瘤、毒物等)的细胞提供能量。已有研究表明,肝纤维化的发病机制中涉及肝星状细胞的活化,伴随着细胞内脂质小滴的消耗,当肝细胞经历自噬,溶酶体的胞内基质将下降。研究还发现肝星状细胞的活化过程中伴随着其自噬水平的升高。本文将就自噬在肝纤维化中的作用做一综述。Autophagy is an intracellular degradative pathway that targets cytosolic components to lysosomes to be degraded for the purposes of maintaining cellular homeostasis and supplying substrates for energy generation. It is present in most of the eukaryotic cells. Autophagy can provide energy for the stressed cell such as inflammatory tumor and poisons. A research has showed that the pathogenesis of hepatic fibrosis refer to the activation of hepatic stellate cells, with consumption of lipid droplet, and accumulation of extra cellular matrix. Researches also have discovered that the autophagy level increased following the activation of hepatic stellate cells, This study will focus on the role autophagy played in the hepatic fibrosis.

关 键 词：细胞自噬 肝星状细胞 肝纤维化 

分 类 号：R575.2[医药卫生—消化系统]