非酒精性脂肪性肝病细胞凋亡的内质网应激启动机制  

Nonalcoholic Fatty Liver Disease of Cell Apoptosis Endoplasmic Reticulum Stress Starting Mechanism

作　　者：陈潇迪[1] 陈东风[1] 王军[1] 樊丽琳[1] 

机构地区：[1]第三军医大学大坪医院野战外科研究所消化内科,重庆400042

出　　处：《现代生物医学进展》2013年第6期1172-1175,共4页Progress in Modern Biomedicine

基　　金：国家自然科学基金项目(81170382)

摘　　要：内质网应激反应,是由于某些因素导致内质网的生理功能紊乱引起的一种细胞自我防御保护机制。内质网应激所诱导的细胞凋亡是近年来新被认识的一种凋亡途径,它不同于既往经典线粒体、死亡受体介导的细胞凋亡。当短暂性内质网应激时,通过激活未折叠蛋白反应来增强机体自我保护及生存能力;而持续性应激状态下,如非酒精性脂肪性肝病所诱导的内质网应激启动一系列凋亡途径如CHOP、JNK、Caspase等,上述凋亡途径可以加速诱导肝细胞凋亡,使NAFLD向肝纤维化方向甚至肝硬化发展。Endoplasmic reticulum stress is a cell-self defense mechanism caused by some factors disordering the physiological fimction of endoplasmic reticulum cells. Endoplasmic reticulum stress induced apoptosis is a new cell apoptosis activation pathway which is different from death receptor pathway and mitochondrial mediated pathway.Transient endoplasmic reticulum stress can activate unfolded protein to enhance viability of cells in exposure of damage factors; And in the sustained endoplasmic reticulum stress condition, such as nonalcoholic fatty liver disease induced endoplasmic reticulum stress activates a series of apoptosis pathway （CHOP, JNK, Cas-pase et al）, inducing liver cell apoptosis, and thus lead NAFLD to liver fibrosis and cirrhosis.

关 键 词：内质网应激 非酒精性 脂肪性肝病 凋亡 

分 类 号：R575.5[医药卫生—消化系统]