title: Bench-to-bedside review: Apoptosis/programmed cell death triggered by traumatic brain injury.
abstract: 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.
authors.affiliation: Department of Critical Care Medicine, University of Pittsburgh School of Medicine, Safar Center for Resuscitation Research, Pittsburgh, PA, USA.
authors.forename: Xiaopeng
authors.initials: X
authors.lastname: Zhang
authors.forename: Yaming
authors.initials: Y
authors.lastname: Chen
authors.forename: Larry W
authors.initials: LW
authors.lastname: Jenkins
authors.forename: Patrick M
authors.initials: PM
authors.lastname: Kochanek
authors.forename: Robert S B
authors.initials: RS
authors.lastname: Clark
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D001930:Brain Injuries / Q000401:mortality / Q000503:physiopathology* / Q000628:therapy; D061945:Caspase Inhibitors; D020169:Caspases / Q000378:metabolism / Q000502:physiology*; D004789:Enzyme Activation; D006801:Humans
chemical_list: D061945:Caspase Inhibitors; D020169:Caspases