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

Joe Springer; Pareshkumar Prajapati; Patrick Sullivan

doi:10.4103/1673-5374.235218

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

Joe Springer, Pareshkumar Prajapati, Patrick Sullivan

Research output: Contribution to journal › Review article › peer-review

25 Scopus citations

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.

Original language	English
Pages (from-to)	1338-1341
Number of pages	4
Journal	Neural Regeneration Research
Volume	13
Issue number	8
DOIs	https://doi.org/10.4103/1673-5374.235218
State	Published - Aug 2018

Bibliographical note

Publisher Copyright:
© 2018 Medknow Publications. All rights reserved.

Funding

Funding: This work was supported by a grant from the Kentucky Spinal Cord and Head Injury Research Trust. Author contributions: JES, PP, and PGS contributed to the review of the literature, generation of the tables, and writing of the manuscript. Conflicts of interest: None declared. Financial support: This work was supported by a grant from the Kentucky Spinal Cord and Head Injury Research Trust. Copyright license agreement: The Copyright License Agreement has been signed by all authors before publication. Plagiarism check: Checked twice by iThenticate. Peer review: Externally peer reviewed. Open access statement: This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-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. Open peer reviewer: Petra Henrich-Noack, Otto von Guericke Uni-versitat Magdeburg, Germany. Additional file: Open peer review report 1.

Funders	Funder number
Kentucky Spinal Cord and Head Injury Research Trust
Kentucky Spinal Cord and Head Injury Research Trust

Keywords

Cyclophilin-D
Cyclosporine A
Functional recovery
Mitochondrial permeability transition
NIM811
Secondary injury
Spinal cord injury
Traumatic brain injury

ASJC Scopus subject areas

Developmental Neuroscience

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10.4103/1673-5374.235218

Cite this

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title = "Targeting the mitochondrial permeability transition pore in traumatic central nervous system injury",

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.",

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AB - 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.

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

Abstract

Bibliographical note

Funding

Keywords

ASJC Scopus subject areas

Access to Document

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