Springer J E, Nottingham S A, McEwen M L, Azbill R D, Jin Y
Department of Anatomy and Neurobiology, Center for Spinal Cord and Head Injury Research, University of Kentucky Medical Center, Lexington 40536, USA.
Clin Chem Lab Med. 2001 Apr;39(4):299-307. doi: 10.1515/CCLM.2001.046.
Apoptotic cell death is a fundamental and highly regulated biological process in which a cell is instructed to participate actively 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 which would target this cell death process. This review will focus on the molecular cell death pathways responsible for generating the apoptotic phenotype, summarize what is currently known about apoptotic signals 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.
凋亡性细胞死亡是一个基本且受到高度调控的生物学过程，在此过程中，细胞被指令主动参与自身的死亡。这种细胞自杀过程由发育和环境信号激活，通常在清除多种组织类型中多余、受损和衰老的细胞方面发挥重要作用。近年来，大量实验研究提供了证据，表明中枢神经系统（CNS）损伤后存在广泛的神经元和胶质细胞凋亡。这些研究表明，损伤诱导的凋亡可在损伤后数小时至数天内被检测到，并且可能导致神经功能障碍。鉴于这些发现，了解控制凋亡的生化信号事件是开发针对这种细胞死亡过程的治疗药物的第一步。本综述将聚焦于负责产生凋亡表型的分子细胞死亡途径，总结目前已知的在受伤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策略来减少这种细胞死亡过程，以此作为促进功能恢复的一种手段。
