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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 wit...

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Detalles Bibliográficos
Autores principales: Zhang, Xiaopeng, Chen, Yaming, Jenkins, Larry W, Kochanek, Patrick M, Clark, Robert SB
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2005
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1065095/
https://www.ncbi.nlm.nih.gov/pubmed/15693986
http://dx.doi.org/10.1186/cc2950
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author Zhang, Xiaopeng
Chen, Yaming
Jenkins, Larry W
Kochanek, Patrick M
Clark, Robert SB
author_facet Zhang, Xiaopeng
Chen, Yaming
Jenkins, Larry W
Kochanek, Patrick M
Clark, Robert SB
author_sort Zhang, Xiaopeng
collection PubMed
description 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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spelling pubmed-10650952005-03-16 Bench-to-bedside review: Apoptosis/programmed cell death triggered by traumatic brain injury Zhang, Xiaopeng Chen, Yaming Jenkins, Larry W Kochanek, Patrick M Clark, Robert SB Crit Care Review 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. BioMed Central 2005 2004-09-03 /pmc/articles/PMC1065095/ /pubmed/15693986 http://dx.doi.org/10.1186/cc2950 Text en Copyright © 2004 BioMed Central Ltd
spellingShingle Review
Zhang, Xiaopeng
Chen, Yaming
Jenkins, Larry W
Kochanek, Patrick M
Clark, Robert SB
Bench-to-bedside review: Apoptosis/programmed cell death triggered by traumatic brain injury
title Bench-to-bedside review: Apoptosis/programmed cell death triggered by traumatic brain injury
title_full Bench-to-bedside review: Apoptosis/programmed cell death triggered by traumatic brain injury
title_fullStr Bench-to-bedside review: Apoptosis/programmed cell death triggered by traumatic brain injury
title_full_unstemmed Bench-to-bedside review: Apoptosis/programmed cell death triggered by traumatic brain injury
title_short Bench-to-bedside review: Apoptosis/programmed cell death triggered by traumatic brain injury
title_sort bench-to-bedside review: apoptosis/programmed cell death triggered by traumatic brain injury
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1065095/
https://www.ncbi.nlm.nih.gov/pubmed/15693986
http://dx.doi.org/10.1186/cc2950
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