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缺血预处理调节内质网应激及促进自噬机制的研究进展
引用本文:杨泽龙,郭婷,陈勇. 缺血预处理调节内质网应激及促进自噬机制的研究进展[J]. 中华实验外科杂志, 2021, 0(1): 190-194
作者姓名:杨泽龙  郭婷  陈勇
作者单位:空军军医大学西京医院肝胆外科;四川大学华西第二医院产科
基金项目:国家自然科学基金(8167030390)。
摘    要: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...

关 键 词:内质网应激  自噬  缺血预处理  缺血再灌注损伤

A review of ischemic preconditioning regulating endoplasmic reticulum stress and promoting autophagy to protect against ischemia-reperfusion injury
Yang Zelong,Guo Ting,Chen Yong. A review of ischemic preconditioning regulating endoplasmic reticulum stress and promoting autophagy to protect against ischemia-reperfusion injury[J]. Chinese Journal of Experimental Surgery, 2021, 0(1): 190-194
Authors:Yang Zelong  Guo Ting  Chen Yong
Affiliation:(Department of Hepatobiliary Surgery,Xijing Hospital,Air Force Military Medical University,Xi′an 710032,China;Department of Obstetrics,West China Second Hospital,Sichuan University,Chengdu 610011,China)
Abstract: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.
Keywords:Endoplasmic reticulum stress  Autophagy  Ischemic preconditioning  Ischemia reperfusion injury
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