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

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.