Zhang Xiaopeng, Chen Yaming, Jenkins Larry W, Kochanek Patrick M, Clark Robert S B
Department of Critical Care Medicine, University of Pittsburgh School of Medicine, Safar Center for Resuscitation Research, Pittsburgh, PA, USA.
Crit Care. 2005 Feb;9(1):66-75. doi: 10.1186/cc2950. Epub 2004 Sep 3.
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.
细胞凋亡,即程序性细胞死亡,是一种生理性细胞死亡形式,对正常胚胎发育及成年生物体中的细胞更新至关重要。越来越多的证据表明,在细胞更新率不高的组织中也可触发细胞凋亡,包括中枢神经系统(CNS)内的组织。事实上,细胞凋亡在急性和慢性中枢神经系统损伤后的迟发性神经元丢失中所起的关键作用正逐渐显现。在本综述中,我们总结了越来越多的证据,这些证据表明从实验模型到人类,创伤性脑损伤(TBI)后都会发生细胞凋亡。这包括TBI后细胞凋亡的识别、凋亡启动因子、凋亡关键调节因子如Bcl-2家族、凋亡关键执行者如半胱天冬酶家族、凋亡的最终途径以及TBI后阻断神经元凋亡的潜在治疗干预措施。