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The mitochondrial permeability transition pore: Molecular nature and role as a target in cardioprotection

The mitochondrial permeability transition (PT) – an abrupt increase permeability of the inner membrane to solutes – is a causative event in ischemia–reperfusion injury of the heart, and the focus of intense research in cardioprotection. The PT is due to opening of the PT pore (PTP), a high conductan...

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Detalles Bibliográficos
Autores principales: Bernardi, Paolo, Di Lisa, Fabio
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Academic Press 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4294587/
https://www.ncbi.nlm.nih.gov/pubmed/25268651
http://dx.doi.org/10.1016/j.yjmcc.2014.09.023
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author Bernardi, Paolo
Di Lisa, Fabio
author_facet Bernardi, Paolo
Di Lisa, Fabio
author_sort Bernardi, Paolo
collection PubMed
description The mitochondrial permeability transition (PT) – an abrupt increase permeability of the inner membrane to solutes – is a causative event in ischemia–reperfusion injury of the heart, and the focus of intense research in cardioprotection. The PT is due to opening of the PT pore (PTP), a high conductance channel that is critically regulated by a variety of pathophysiological effectors. Very recent work indicates that the PTP forms from the F-ATP synthase, which would switch from an energy-conserving to an energy-dissipating device. This review provides an update on the current debate on how this transition is achieved, and on the PTP as a target for therapeutic intervention. This article is part of a Special Issue entitled "Mitochondria: from basic mitochondrial biology to cardiovascular disease".
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spelling pubmed-42945872015-01-21 The mitochondrial permeability transition pore: Molecular nature and role as a target in cardioprotection Bernardi, Paolo Di Lisa, Fabio J Mol Cell Cardiol Review Article The mitochondrial permeability transition (PT) – an abrupt increase permeability of the inner membrane to solutes – is a causative event in ischemia–reperfusion injury of the heart, and the focus of intense research in cardioprotection. The PT is due to opening of the PT pore (PTP), a high conductance channel that is critically regulated by a variety of pathophysiological effectors. Very recent work indicates that the PTP forms from the F-ATP synthase, which would switch from an energy-conserving to an energy-dissipating device. This review provides an update on the current debate on how this transition is achieved, and on the PTP as a target for therapeutic intervention. This article is part of a Special Issue entitled "Mitochondria: from basic mitochondrial biology to cardiovascular disease". Academic Press 2015-01 /pmc/articles/PMC4294587/ /pubmed/25268651 http://dx.doi.org/10.1016/j.yjmcc.2014.09.023 Text en © 2014 The Authors http://creativecommons.org/licenses/by-nc-nd/3.0/ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/3.0/).
spellingShingle Review Article
Bernardi, Paolo
Di Lisa, Fabio
The mitochondrial permeability transition pore: Molecular nature and role as a target in cardioprotection
title The mitochondrial permeability transition pore: Molecular nature and role as a target in cardioprotection
title_full The mitochondrial permeability transition pore: Molecular nature and role as a target in cardioprotection
title_fullStr The mitochondrial permeability transition pore: Molecular nature and role as a target in cardioprotection
title_full_unstemmed The mitochondrial permeability transition pore: Molecular nature and role as a target in cardioprotection
title_short The mitochondrial permeability transition pore: Molecular nature and role as a target in cardioprotection
title_sort mitochondrial permeability transition pore: molecular nature and role as a target in cardioprotection
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4294587/
https://www.ncbi.nlm.nih.gov/pubmed/25268651
http://dx.doi.org/10.1016/j.yjmcc.2014.09.023
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