缺血预处理调节内质网应激及促进自噬机制的研究进展

A review of ischemic preconditioning regulating endoplasmic reticulum stress and promoting autophagy to protect against ischemia-reperfusion injury

缺血预处理(IPC)对于缺血再灌注损伤(IRI)发生后更迅速的恢复生理功能和组织结构和减少损伤具有重要的作用。细胞受到外界刺激后,内质网应激(ERS)启动,可以通过减少未折叠蛋白的累积并增加未折叠蛋白的降解,保护内质网稳态,泛素化降解系统也参与其中,但当细胞受到外界刺激持续或者过强时,ERS和泛素化降解系统无法消除未折叠蛋白时,自噬的激活可作为恢复内质网稳态的最后防线。除此之外,目前也有相关研究表明ERS可促进细胞自噬,维持细胞存活及内质网稳态,参与多种生理及病理过程。本综述将缺血预处理调节ERS相关通路促进自噬保护IRI的相关研究进行归纳,以期为缺血预处理保护IRI机制主题相关的科学研究提供参考。

Ischemia preconditioning(IPC)plays an important role in restoring physiological function and tissue structure and reducing damage after the occurrence of ischemia reperfusion injury(IRI).Endoplasmic reticulum stress(ERS)contributes to endoplasmic reticulum homeostasis by reducing the accumulation of unfolded proteins and increasing the degradation of unfolded proteins.The ubiquitin degradation system participates in the degradation of unfolded proteins too.But if the ERS and ubiquitin degradation system can′t maintain endoplasmic reticulum homeostasis when the external stimulus persists because of their limited ability,the activation of autophagy may act as the last and effective option to restore the endoplasmic reticulum homeostasis.This review summarizes the role of IPC in regulating ERS and promoting autophagy to protect organs and cells from IRI,with a view of providing a reference for further studies.