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JAK2/STAT3信号通路与脑缺血-再灌注损伤相关性的研究进展
作者:杨柳  陈蓓蕾  于海龙  李军 
单位:大连医科大学 研究生院, 辽宁 大连 116044
关键词:JAK2/STAT3信号通路 脑缺血-再灌注损伤 凋亡 
分类号:R743.31
出版年·卷·期(页码):2018·37·第一期(169-173)
摘要:

神经细胞凋亡是急性脑缺血-再灌注损伤的重要病理机制之一,寻找抑制此病理过程的有效方法一直是研究者关注的热点。JAK2/STAT3信号通路是近年来新发现的与神经细胞病理损伤相关的信号通路,其在中枢神经系统中的主要作用是参与神经细胞存活、增殖、分化、凋亡的过程。已有的研究表明,JAK2/STAT3信号通路与脑缺血-再灌注后神经细胞凋亡密切相关。本文就该信号通路与脑缺血-再灌注后病理性机制的研究进展进行述评,为脑缺血-再灌注损伤中神经保护提供新的潜在靶点。

Neuronal apoptosis is one of the important pathologic mechanisms of acute cerebral ischemia-reperfusion injury. It is a hot topic to find an effective method to inhibit this pathological process. JAK2/STAT3 signaling pathway is a newly discovered signal pathway related to the pathological damage of neuronal. Its main role in the central nervous system is to participate the process of neuronal survival,proliferation, differentiation and apoptosis.Previous studies have shown that JAK2/STAT3 signal pathway is closely related to neuronal apoptosis after cerebral ischemia-reperfusion injury. This article focus on the pathology and pathogenesis of cerebral ischemia-reperfusion injury and provides new potential targets of neuroprotection for cerebral ischemia-reperfusion injury.

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