Evidence to support mitochondrial neuroprotection, in severe traumatic brain injury

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• 作者：Shyam Gajavelli ; Vishal K. Sinha…
• 关键词：Mitochondrial dynamics ; Hypoxia ; Cyclosporine A ; Mitochondrial dysfunction ; Penetrating traumatic brain injury ; Secondary brain injury ; KTP
• 刊名：Journal of Bioenergetics and Biomembranes
• 出版年：2015
• 出版时间：April 2015
• 年：2015
• 卷：47
• 期：1-2
• 页码：133-148
• 全文大小：1,654 KB
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• 刊物类别：Chemistry and Materials Science
• 刊物主题：Chemistry
  Bioorganic Chemistry
  Biochemistry
  Animal Anatomy, Morphology and Histology
  Animal Biochemistry
  Organic Chemistry
  
• 出版者：Springer New York
• ISSN：1573-6881

文摘

Traumatic brain injury (TBI) is still the leading cause of disability in young adults worldwide. The major mechanisms -diffuse axonal injury, cerebral contusion, ischemic neurological damage, and intracranial hematomas have all been shown to be associated with mitochondrial dysfunction in some form. Mitochondrial dysfunction in TBI patients is an active area of research, and attempts to manipulate neuronal/astrocytic metabolism to improve outcomes have been met with limited translational success. Previously, several preclinical and clinical studies on TBI induced mitochondrial dysfunction have focused on opening of the mitochondrial permeability transition pore (PTP), consequent neurodegeneration and attempts to mitigate this degeneration with cyclosporine A (CsA) or analogous drugs, and have been unsuccessful. Recent insights into normal mitochondrial dynamics and into diseases such as inherited mitochondrial neuropathies, sepsis and organ failure could provide novel opportunities to develop mitochondria-based neuroprotective treatments that could improve severe TBI outcomes. This review summarizes those aspects of mitochondrial dysfunction underlying TBI pathology with special attention to models of penetrating traumatic brain injury, an epidemic in modern American society.