内质网应激在心肌缺血预处理中的作用  

The roles of endoplasmic reticulum stress in cardioprotection induced by ischemia preconditioning

作　　者：陈满丽[1] 陈立建[1] 顾尔伟[1] 

机构地区：[1]安徽医科大学第一附属医院麻醉科,合肥230032

出　　处：《国际麻醉学与复苏杂志》2015年第8期754-759,共6页International Journal of Anesthesiology and Resuscitation

基　　金：安徽省自然科学基金（1308085MH118）

摘　　要：背景内质网应激（endoplasmic reticulumstress，ERS）是细胞内对抗氧化应激、钙超载、能量耗竭的一种适应性反应，适度的ERS通过促生存途径保护细胞。心肌缺血，再灌注（ischemia／reperfusion，I／R）期间诱导过度的ERS发生，导致心肌损伤。心肌缺血预处理（ischemiapreconditioning，IPC）可通过调节ERS发挥心肌保护作用。目的综述ERS调节心肌IPC的作用及其影响因素。内容系统阐述ERS在调节细胞生存与凋亡、心肌I／R过程中的作用及IPC调节ERS的机制。趋向心肌IPC通过调节ERS反应来发挥心肌保护效应受多方面因素影响，其具体机制仍有待进一步研究。Background Endoplasmic reticulum stress（ERS） is a type of cellular adaptive reaction against oxidative stress, calcium overload and ATP depletion. Mild ERS protects myocardium via pro-survival pathways. Myocardium ischemia/reperfusion （I/ R） would induce prolonged ERS, which may result in irreversible injury. ERS is involved in the eardioprotection induced by ischemia preconditioning （IPC）. Objective This review focused on the factors which regulate ERS mediated by IPC and demonstrated its possible mechanisms. Content To discuss the roles of ERS in cells survival, apotosis and cardioprotection induced by IPC. Trend There are many factors involved in the cardioprotection induced by IPC via regulating ERS, and its mechanisms need further studies.

关 键 词：内质网应激 缺血/再灌注 缺血预处理 心肌保护 

分 类 号：R614[医药卫生—麻醉学]