Journal
CRITICAL CARE
Volume 9, Issue 1, Pages 66-75Publisher
BIOMED CENTRAL LTD
DOI: 10.1186/cc2950
Keywords
apoptosis, Bcl-2, caspase; head injury, programmed cell death, traumatic brain injury
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Funding
- NINDS NIH HHS [R01 NS38620, P50 NS30318, R01 NS038620, P50 NS030318] Funding Source: Medline
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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.
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