Mitochondrial damage and dysfunction in traumatic brain injury
Mitochondrial damage and dysfunction in traumatic brain injury
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DOI：
10.1016/j.mito.2004.07.021
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发表时间：
2004-09-01
期刊：
影响因子：
4.4
通讯作者：
McIntosh, TK
中科院分区：
文献类型：
--
作者：
Lifshitz, J;Sullivan, PG;McIntosh, TK
与创伤性脑损伤（TBI）相关的持久认知缺陷和组织病理学可能由线粒体群体的损伤引起，其引发在临床和实验TBI中观察到的代谢功能障碍。线粒体体内结构损伤的轶事证据证实了代谢和生理功能障碍，其消耗底物并促进自由基产生。过多的钙病理学差异性地破坏异质性线粒体群体，使得TBI后钙敏感性增加。正在进行的病理学可能升级到包括影响线粒体功能并促进细胞死亡的蛋白质和DNA氧化。因此，体内TBI损害（如果不是消除的话）线粒体群体，这取决于损伤的严重程度，剩余的群体在细胞病理学之后为存活或修复提供代谢支持。随着对损伤后线粒体群体的大量了解，针对线粒体的治疗干预可能会延迟或预防导致长期细胞死亡和神经行为障碍的继发性级联反应。(C)2004年Elsevier B.V.和线粒体研究学会。All rights reserved.
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.