Bench-to-bedside review: Apoptosis/programmed cell death triggered by traumatic brain injury.
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.
Zhang
Xiaopeng
X
Department of Critical Care Medicine, University of Pittsburgh School of Medicine, Safar Center for Resuscitation Research, Pittsburgh, PA, USA.
Chen
Yaming
Y
Jenkins
Larry W
LW
Kochanek
Patrick M
PM
Clark
Robert S B
RS
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
D061945:Caspase Inhibitors; D020169:Caspases