内质网应激与缺血性脑损伤

Endoplasmic Reticulum Stress and Cerebral Ischemic Injury

内质网应激是内质网内未折叠或错误折叠蛋白积聚所致。作为对内质网应激的响应,细胞形成了一条称为未折叠蛋白反应(UPR)的自我保护信号转导通路。然而,如果脑缺血诱导的内质网应激严重且持续时间长,UPR最终会启动细胞凋亡通路,导致神经元死亡。文章对脑缺血再灌注诱导内质网应激和UPR的研究进展做了综述。

Endoplasmic reticulum （ER） stress results from the accumulation of unfolded or misfolded proteins in the ER. In response to ER stress, cells have developed a self-protective signal transduction pathway termed the unfolded protein response （UPR）. However, if ER stress induced by cerebral ischemia is severe and prolonged, UPR ultimately initiates an apoptotic pathway, resulting in neuronal death. This article reviews the recent progress in ER stress and UPR induced by cerebral ischemic-reperfusion.