内质网应激和自噬的交互作用及其在阿尔茨海默病进展与防治中的作用  

Crosstalk between endoplasmic reticulum stress and autophagy andits role in pathogenesis and prevention of Alzheimer’s disease

作　　者：黄倩倩 温彬宇[2] 闫妍[2] 赵永烈 马涛[2] HUANG Qian-qian;WEN Bin-yu;YAN Yan;ZHAO Yong-lie;MA Tao(Dept of Encephalopathy,the Third Affiliated Hospital,Beijing University of Chinese Medicine,Beijing 100029,China;Research Center of Dongfang Hospital,Beijing University of Chinese Medicine,Beijing 100078,China)

机构地区：[1]北京中医药大学第三附属医院脑病科,北京100029 [2]北京中医药大学东方医院实验中心,北京100078

出　　处：《中国药理学通报》2018年第11期1500-1504,共5页Chinese Pharmacological Bulletin

基　　金：国家自然科学基金资助项目(No 81673929)

摘　　要：阿尔茨海默病(Alzheimer’s disease, AD)中内质网应激(endoplasmic reticulum stress, ERS)的持续性激活和自噬功能障碍,导致ERS与自噬之间的交互作用由适应性、保护性,逐渐转变为持续性、破坏性,是推动AD病程进展的关键因素,由此成为AD防治的重要靶标。未折叠蛋白反应(unfolded protein response, UPR)相关信号通路在ERS与自噬交互推动AD进展中发挥核心作用。该文就ERS与自噬交互效应在AD进展防治中的作用及相关分子机制做一综述。The chronic activation of endoplasmic reticulum stress(ERS)and impaired autophagy in Alzheimer’s disease(AD)could change the crosstalk between ERS and autophagy from an adaptive protective mechanism against the injury to a continuous and destructive one.The latter,in hence,is a key factor for driving AD development,becoming a valuble therapeutic target for AD treatment.The pathways related to unfolded protein response(UPR)play a key role in the crosstalk between ERS and autophagy,which exacerbates AD progress.This paper summarizes the recent research outcome about the crosstalk between ERS and autophagy,and its role in AD development and treatment.

关 键 词：阿尔茨海默病 内质网应激 自噬 未折叠蛋白反应 交互作用 Β淀粉样蛋白 

分 类 号：R-05[医药卫生] R329.24