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REVIEW
Year : 2018  |  Volume : 13  |  Issue : 8  |  Page : 1338-1341

Targeting the mitochondrial permeability transition pore in traumatic central nervous system injury


Spinal Cord and Brain Injury Research Center, Department of Neuroscience, University of Kentucky, Lexington, KY, USA

Correspondence Address:
Joe E Springer
Spinal Cord and Brain Injury Research Center, Department of Neuroscience, University of Kentucky, Lexington, KY
USA
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Source of Support: This work was supported by a grant from the Kentucky Spinal Cord and Head Injury Research Trust, Conflict of Interest: None


DOI: 10.4103/1673-5374.235218

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The mitochondrion serves many functions in the central nervous system (CNS) and other organs beyond the well-recognized role of adenosine triphosphate (ATP) production. This includes calcium-dependent cell signaling, regulation of gene expression, synthesis and release of cytotoxic reactive oxygen species, and the release of cytochrome c and other apoptotic cell death factors. Traumatic injury to the CNS results in a rapid and, in some cases, sustained loss of mitochondrial function. One consequence of compromised mitochondrial function is induction of the mitochondrial permeability transition (mPT) state due to formation of the cyclosporine A sensitive permeability transition pore (mPTP). In this mini-review, we summarize evidence supporting the involvement of the mPTP as a mediator of mitochondrial and cellular demise following CNS traumatic injury and discuss the beneficial effects and limitations of the current ex­perimental strategies targeting the mPTP.


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