Abstract
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 ex-perimental strategies targeting the mPTP.
Document Type
Review
Publication Date
8-2018
Digital Object Identifier (DOI)
https://doi.org/10.4103/1673-5374.235218
Funding Information
This work was supported by a grant from the Kentucky Spinal Cord and Head Injury Research Trust.
Related Content
Additional file: Open peer review report 1.
Repository Citation
Springer, Joe E.; Prajapati, Pareshkumar; and Sullivan, Patrick G., "Targeting the Mitochondrial Permeability Transition Pore in Traumatic Central Nervous System Injury" (2018). Spinal Cord and Brain Injury Research Center Faculty Publications. 21.
https://uknowledge.uky.edu/scobirc_facpub/21
Additional file: Open peer review report 1.
Notes/Citation Information
Published in Neural Regeneration Research, v. 13, issue 8, p. 1338-1341.
This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution-Non-Commercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms.