Bench-to-bedside review: Apoptosis/programmed cell death triggered by traumatic brain injury

被引:179
作者
Zhang, XP
Chen, YM
Jenkins, LW
Kochanek, PM
Clark, RSB [1 ]
机构
[1] Univ Pittsburgh, Sch Med, Dept Crit Care Med, Safar Ctr Resuscitat Res, Pittsburgh, PA 15261 USA
[2] Univ Pittsburgh, Sch Med, Dept Pediat, Safar Ctr Resuscitat Res, Pittsburgh, PA 15261 USA
[3] Univ Pittsburgh, Sch Med, Dept Neurol Surg, Safar Ctr Resuscitat Res, Pittsburgh, PA 15261 USA
来源
CRITICAL CARE | 2005年 / 9卷 / 01期
关键词
apoptosis; Bcl-2; caspase; head injury; programmed cell death; traumatic brain injury;
D O I
10.1186/cc2950
中图分类号
R4 [临床医学];
学科分类号
1002 ; 100602 ;
摘要
Apoptosis, or programmed cell death, is a physiological form of cell death that is important for normal embryologic development and cell turnover in adult organisms. Cumulative evidence suggests that apoptosis can also be triggered in tissues without a high rate of cell turnover, including those within the central nervous system (CNS). In fact, a crucial role for apoptosis in delayed neuronal loss after both acute and chronic CNS injury is emerging. In the current review we summarize the growing evidence that apoptosis occurs after traumatic brain injury (TBI), from experimental models to humans. This includes the identification of apoptosis after TBI, initiators of apoptosis, key modulators of apoptosis such as the Bcl-2 family, key executioners of apoptosis such as the caspase family, final pathways of apoptosis, and potential therapeutic interventions for blocking neuronal apoptosis after TBI.
引用
收藏
页码:66 / 75
页数:10
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