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

• Published in: Critical care (London, England) Vol. 9; no. 1; pp. 66 - 75
• Main Authors: Zhang, Xiaopeng, Chen, Yaming, Jenkins, Larry W, Kochanek, Patrick M, Clark, Robert S B
• Format: Journal Article
• Language: English
• Published: England National Library of Medicine - MEDLINE Abstracts 01-02-2005; BioMed Central Ltd; BioMed Central
• Subjects: Animals; Apoptosis - physiology; Brain Injuries - mortality; Brain Injuries - physiopathology; Brain Injuries - therapy; Caspase Inhibitors; Caspases - metabolism; Caspases - physiology; Enzyme Activation; Humans; Review
• ISSN: 1364-8535; 1466-609X
• DOI: 10.1186/cc2950

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.