Apoptotic cell death following traumatic injury to the central nervous system.
Apoptotic cell death following traumatic injury to the central nervous system.
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DOI：
10.5483/bmbrep.2002.35.1.094
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发表时间：
2002-01
期刊：
影响因子：
--
通讯作者：
J. Springer
中科院分区：
文献类型：
--
作者：
J. Springer
细胞凋亡是一个基本的和高度调节的生物过程，其中细胞被指示积极参与其自身的死亡。这种细胞自杀过程由发育和环境线索激活，通常在消除许多组织类型的多余，受损和衰老细胞中起重要作用。近年来，大量的实验研究表明，中枢神经系统（CNS）损伤后存在广泛的神经元和神经胶质细胞凋亡。这些研究表明，损伤诱导的细胞凋亡可在损伤后数小时至数天内检测到，并可能导致神经功能障碍。鉴于这些发现，了解控制细胞凋亡的生化信号事件是开发靶向这种细胞死亡过程的治疗剂的第一步。这篇评论将集中在分子细胞死亡途径，负责产生凋亡表型。它还将总结什么是目前已知的在受损的中枢神经系统中被激活的凋亡信号，以及可能采取哪些潜在的策略来减少这种细胞死亡过程，以促进功能恢复。
Apoptotic cell death is a fundamental and highly regulated biological process in which a cell is instructed to actively participate in its own demise. This process of cellular suicide is activated by developmental and environmental cues and normally plays an essential role in eliminating superfluous, damaged, and senescent cells of many tissue types. In recent years, a number of experimental studies have provided evidence of widespread neuronal and glial apoptosis following injury to the central nervous system (CNS). These studies indicate that injury-induced apoptosis can be detected from hours to days following injury and may contribute to neurological dysfunction. Given these findings, understanding the biochemical signaling events controlling apoptosis is a first step towards developing therapeutic agents that target this cell death process. This review will focus on molecular cell death pathways that are responsible for generating the apoptotic phenotype. It will also summarize what is currently known about the apoptotic signals that are activated in the injured CNS, and what potential strategies might be pursued to reduce this cell death process as a means to promote functional recovery.