Mitochondrial damage and dysfunction in traumatic brain injury
(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)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/257786
- author
- Lifshitz, J ; Sullivan, PG ; Hovda, DA ; Wieloch, Tadeusz LU and McIntosh, TK
- organization
- publishing date
- 2004
- 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
- additional info
- The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Laboratory for Experimental Brain Research (013041000)
- id
- 9e199289-6c5d-4b1a-88e9-2e37d1315f33 (old id 257786)
- date added to LUP
- 2016-04-01 11:38:32
- date last changed
- 2022-03-28 00:53:18
@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}}, keywords = {{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}}, doi = {{10.1016/j.mito.2004.07.021}}, volume = {{4}}, year = {{2004}}, }