内质网应激参与调节心肌缺血/再灌注损伤的新进展  

The role of endoplasmic reticulum stress in myocardium ischemia reperfusion injury

作　　者：邹麓[1] 贾大林[1] 

机构地区：[1]中国医科大学附属第一医院心血管内科,辽宁沈阳110001

出　　处：《解剖科学进展》2016年第2期207-209,共3页Progress of Anatomical Sciences

基　　金：国家自然科学基金(81401413)

摘　　要：缺血/再灌注损伤(IRI)是恢复心肌血流再灌注对心肌造成的二次损伤,其病理生理过程涉及凋亡、氧化应激、钙超载、自噬等多个方面。内质网应激(ERS)是细胞对不良刺激的一种适应性应答反应,在IRI过程中被激活,具有"促生存"和"促凋亡"双重作用。由于ERS与凋亡、氧化应激等IRI的多个病理生理过程密切相关,故调控ERS有望成为减轻IRI的新靶点。Ischemia reperfusion injury（IRI） is defined as the injury caused by the process of restoring blood flow to the ischemic myocardium, which paradoxically reduces the beneficial effect of myocardial reperfusion. Apoptosis, oxidative stress, Ca2＋ overload and autophagy are involved in this process. Endoplasmie reticulum stress（ERS） is a respond to perturbations in ER function, which is activated in IRI and critical for cell survival. The role of ERS in IRI has not been clearly clarified, but is closely related to apoptosis, autophagy and oxidatitive stress.

关 键 词：缺血/再灌注损伤 内质网应激 心肌 病理生理过程 调节 氧化应激 血流再灌注 促凋亡 

分 类 号：R541.4[医药卫生—心血管疾病]