Cellular and molecular events underlying ischemia-induced neuronal apoptosis

被引:64
|
作者
Zheng, Z
Zhao, H
Steinberg, GK
Yenari, AA
机构
[1] Stanford Univ, Sch Med, Dept Neurosurg, Stanford, CA 94305 USA
[2] Stanford Univ, Sch Med, Dept Neurol, Stanford, CA 94305 USA
[3] Stanford Univ, Sch Med, Dept Neurol Sci, Stanford, CA 94305 USA
关键词
D O I
10.1358/dnp.2003.16.8.829348
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Neurons subjected to ischemia undergo necrosis or apoptosis depending on their anatomic distribution and the severity and duration of ischemia. Recent work has shown that apoptosis can occur in some settings, primarily within the ischemic penumbra. It is recognized that both mitochondrial and death-receptor pathways are involved in the transduction of apoptotic signals in the context of cerebral ischemia. Recent data also highlight the pivotal role of caspase 3 in the execution of ischemia-induced apoptosis, although a caspase-independent pathway is gaining increasing attention. In this review, we examine some of these findings and their potential therapeutic implications for ischemic stroke. (C) 2003 Prous Science. All rights reserved.
引用
收藏
页码:497 / 503
页数:7
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