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Mitochondrial damage and dysfunction in traumatic brain injury

Lifshitz, J; Sullivan, PG; Hovda, DA; Wieloch, Tadeusz LU and McIntosh, TK (2004) In Mitochondrion 4(5-6). p.705-713
Abstract
The enduring cognitive deficits and histopathology associated with traumatic brain injury (TBI) may arise from damage to mitochondrial populations, which initiates the metabolic dysfunction observed in clinical and experimental TBI. The anecdotal evidence for in vivo structural damage to mitochondria corroborates metabolic and physiologic dysfunction, which depletes substrates and promotes free radical generation. Excessive calcium pathology differentially disrupts the heterogeneous mitochondrial population, such that calcium sensitivity increases after TBI. The ongoing pathology may escalate to include protein and DNA oxidation that impacts mitochondrial function and promotes cell death. Thus, in vivo TBI damages, if not eliminates,... (More)
The enduring cognitive deficits and histopathology associated with traumatic brain injury (TBI) may arise from damage to mitochondrial populations, which initiates the metabolic dysfunction observed in clinical and experimental TBI. The anecdotal evidence for in vivo structural damage to mitochondria corroborates metabolic and physiologic dysfunction, which depletes substrates and promotes free radical generation. Excessive calcium pathology differentially disrupts the heterogeneous mitochondrial population, such that calcium sensitivity increases after TBI. The ongoing pathology may escalate to include protein and DNA oxidation that impacts mitochondrial function and promotes cell death. Thus, in vivo TBI damages, if not eliminates, mitochondrial populations depending on injury severity, with the remaining population left to provide metabolic support for survival or repair in the wake of cellular pathology. With a considerable understanding of post-injury mitochondrial populations, therapeutic interventions targeted to the mitochondria may delay or prevent secondary cascades that lead to long-term cell death and neurobehavioral disability. (C) 2004 Elsevier B.V. and Mitochondria Research Society. All rights reserved. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
metabolism, brain injury, mitochondria
in
Mitochondrion
volume
4
issue
5-6
pages
705 - 713
publisher
Elsevier
external identifiers
  • wos:000226172600031
  • pmid:16120426
  • scopus:10644267592
ISSN
1567-7249
DOI
10.1016/j.mito.2004.07.021
language
English
LU publication?
yes
id
9e199289-6c5d-4b1a-88e9-2e37d1315f33 (old id 257786)
date added to LUP
2007-10-24 18:48:48
date last changed
2017-11-12 03:18:51
@article{9e199289-6c5d-4b1a-88e9-2e37d1315f33,
  abstract     = {The enduring cognitive deficits and histopathology associated with traumatic brain injury (TBI) may arise from damage to mitochondrial populations, which initiates the metabolic dysfunction observed in clinical and experimental TBI. The anecdotal evidence for in vivo structural damage to mitochondria corroborates metabolic and physiologic dysfunction, which depletes substrates and promotes free radical generation. Excessive calcium pathology differentially disrupts the heterogeneous mitochondrial population, such that calcium sensitivity increases after TBI. The ongoing pathology may escalate to include protein and DNA oxidation that impacts mitochondrial function and promotes cell death. Thus, in vivo TBI damages, if not eliminates, mitochondrial populations depending on injury severity, with the remaining population left to provide metabolic support for survival or repair in the wake of cellular pathology. With a considerable understanding of post-injury mitochondrial populations, therapeutic interventions targeted to the mitochondria may delay or prevent secondary cascades that lead to long-term cell death and neurobehavioral disability. (C) 2004 Elsevier B.V. and Mitochondria Research Society. All rights reserved.},
  author       = {Lifshitz, J and Sullivan, PG and Hovda, DA and Wieloch, Tadeusz and McIntosh, TK},
  issn         = {1567-7249},
  keyword      = {metabolism,brain injury,mitochondria},
  language     = {eng},
  number       = {5-6},
  pages        = {705--713},
  publisher    = {Elsevier},
  series       = {Mitochondrion},
  title        = {Mitochondrial damage and dysfunction in traumatic brain injury},
  url          = {http://dx.doi.org/10.1016/j.mito.2004.07.021},
  volume       = {4},
  year         = {2004},
}