内质网应激:急性缺血性卒中的潜在治疗靶点  

Endoplasmic reticulum stress:a potential therapeutic target for acute ischemic stroke

作　　者：张艳[1] 揭春晓 胡诗俊 彭定天 黄治坤 程道宾[1] Zhang Yan;Jie Chunxiao;Hu Shijun;Peng Dingtian;Huang Zhikun;Cheng Daobin(Department of Neurology,the First Affiliated Hospital of Guangxi Medical University,Nanning 530021,China;Department of Neurology,Hainan Provincial People's Hospital,Haikou 570100,China;Department of Neurology,Wuming Hospital Affiliated to Guangxi Medical University,Nanning 530121,China)

机构地区：[1]广西医科大学第一附属医院神经内科,南宁530021 [2]海南省人民医院神经内科,海口570100 [3]广西医科大学附属武鸣医院神经内科,南宁530121

出　　处：《国际脑血管病杂志》2020年第12期943-948,共6页International Journal of Cerebrovascular Diseases

基　　金：海南省自然科学基金青年基金项目(819QN348)。

摘　　要：内质网是蛋白质合成、折叠和翻译后修饰以及Ca2+动态平衡的场所。急性缺血性卒中造成的缺血缺氧等因素会诱导内质网应激(endoplasmic reticulum stress,ERS)的发生。轻度ERS可恢复细胞内环境的稳定以及增强细胞的生存能力,但严重且持续的ERS则会诱导细胞凋亡或引起坏死性损伤。文章主要介绍促进细胞内源性生存的可能途径以及ERS诱导细胞死亡的可能机制,探讨急性缺血性卒中的潜在治疗靶点。The endoplasmic reticulum is the site of protein synthesis,folding,post-translational modification,and Ca2+homeostasis.Factors such as ischemia and hypoxia caused by acute ischemic stroke can induce the occurrence of endoplasmic reticulum stress(ERS).Mild ERS can restore the stability of the intracellular environment and enhance cell viability,but severe and continuous ERS can induce cell apoptosis or cause necrotic damage.This article mainly introduces the possible pathways to promote cell endogenous survival and the possible mechanism of ERS-induced cell death,and explores potential therapeutic targets for acute ischemic stroke.

关 键 词：卒中 脑缺血 内质网应激 未折叠蛋白反应 细胞死亡 细胞凋亡 信号转导 

分 类 号：R743.3[医药卫生—神经病学与精神病学]