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细胞内丝裂原活化蛋白激酶信号通路与脑缺血后神经元凋亡 被引量:5

Mitogen-activated protein kinase signaling pathways and nemunai apoptosis after cerebral ischemia
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摘要 脑缺血可导致梗死核心区细胞坏死和缺血半暗带细胞凋亡。脑缺血后,丝裂原活化蛋白激酶(mitogen—activated protein kinases,MAPKs)信号通路被激活,引起程序性细胞死亡,包括细胞凋亡。文章就MAPKs信号家族与脑缺血后神经元凋亡的关系进行了综述。 Cerebral ischemia can induce cell necrosis in core of the infarction, and apoptosis in the ischemic penumbra. The mitogen-activated protein kinases (MAPKs) signaling pathways are activated after cerebral ischemia, causing programmed cell death, including apoptosis. This article reviews the relationship between the MAPKs signaling family and neuronal apoptosis after cerebral ischemia.
作者 谢君 张智博
出处 《国际脑血管病杂志》 2015年第6期464-468,共5页 International Journal of Cerebrovascular Diseases
关键词 脑缺血 p38有丝分裂原激活蛋白激酶 信号转导 MAP激酶信号系统 细胞凋亡 Brain Ischemia p38 Mitogen-Activated Protein Kinases Signal Transduction MAP Kinase Signaling System Apoptosis.
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