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The mPTP and its regulatory proteins: final common targets of signalling pathways for protection against necrosis

The mPTP and its regulatory proteins: final common targets of signalling pathways for protection... The mitochondrial permeability transition pore (mPTP) is a non-selective, large-conductance channel that is closed under physiological conditions. Opening of the mPTP, leading to abolition of mitochondrial functions, is a major mechanism of myocyte necrosis by ischaemia/reperfusion, and direct inhibition of mPTP opening by use of pharmacological or genetic manipulations limits infarct size in vivo. Multiple pro-survival signal pathways commonly target the mPTP and inhibit its opening. Although the molecular structure of the mPTP has not been established, recent studies have characterized roles of each mPTP subunit and functions of several proteins directly interacting with the mPTP. This article briefly describes the understanding of mPTP regulation and interaction of the mPTP with four proteins (hexokinase II, glycogen synthase kinase-3β, signal transducer and activator of transcription 3, and sirtuin 3) that are downstream of signal pathways relevant to protection from ischaemia/reperfusion injury. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Cardiovascular Research Oxford University Press

The mPTP and its regulatory proteins: final common targets of signalling pathways for protection against necrosis

Cardiovascular Research , Volume 94 (2) – May 1, 2012

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References (113)

Publisher
Oxford University Press
Copyright
Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2011. For permissions please email: journals.permissions@oup.com.
Subject
REVIEWS: SPOTLIGHT ON REDUCING MYOCARDIAL ISCHAEMIA/REPERFUSION INJURY
ISSN
0008-6363
eISSN
1755-3245
DOI
10.1093/cvr/cvr302
pmid
22072634
Publisher site
See Article on Publisher Site

Abstract

The mitochondrial permeability transition pore (mPTP) is a non-selective, large-conductance channel that is closed under physiological conditions. Opening of the mPTP, leading to abolition of mitochondrial functions, is a major mechanism of myocyte necrosis by ischaemia/reperfusion, and direct inhibition of mPTP opening by use of pharmacological or genetic manipulations limits infarct size in vivo. Multiple pro-survival signal pathways commonly target the mPTP and inhibit its opening. Although the molecular structure of the mPTP has not been established, recent studies have characterized roles of each mPTP subunit and functions of several proteins directly interacting with the mPTP. This article briefly describes the understanding of mPTP regulation and interaction of the mPTP with four proteins (hexokinase II, glycogen synthase kinase-3β, signal transducer and activator of transcription 3, and sirtuin 3) that are downstream of signal pathways relevant to protection from ischaemia/reperfusion injury.

Journal

Cardiovascular ResearchOxford University Press

Published: May 1, 2012

Keywords: Mitochondria Signal transduction Hexokinase Glycogen synthase kinase-3β Mitochondrial permeability transition pore

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