SIRT3 in Cardiac Physiology and Disease

Functional defects in mitochondrial biology causally contribute to various human diseases, including cardiovascular disease. Impairment in oxidative phosphorylation, mitochondrial oxidative stress, and increased opening of the mitochondrial permeability transition pore add to the underlying mechanis...

Full description

Bibliographic Details
Main Authors:	Koentges, Christoph, Bode, Christoph, Bugger, Heiko
Format:	Online
Language:	English
Published:	Frontiers Media S.A. 2016
Online Access:	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5061741/

id	pubmed-5061741
recordtype	oai_dc
spelling	pubmed-50617412016-10-27 SIRT3 in Cardiac Physiology and Disease Koentges, Christoph Bode, Christoph Bugger, Heiko Cardiovascular Medicine Functional defects in mitochondrial biology causally contribute to various human diseases, including cardiovascular disease. Impairment in oxidative phosphorylation, mitochondrial oxidative stress, and increased opening of the mitochondrial permeability transition pore add to the underlying mechanisms of heart failure or myocardial ischemia–reperfusion (IR) injury. Recent evidence demonstrated that the mitochondrial NAD+-dependent deacetylase sirtuin 3 (SIRT3) may regulate these mitochondrial functions by reversible protein lysine deacetylation. Loss of function studies demonstrated a role of impaired SIRT3 activity in the pathogenesis of myocardial IR injury as well as in the development of cardiac hypertrophy and the transition into heart failure. Gain of function studies and treatment approaches increasing mitochondrial NAD+ availability that ameliorate these cardiac pathologies have led to the proposal that activation of SIRT3 may represent a promising therapeutic strategy to improve mitochondrial derangements in various cardiac pathologies. In the current review, we will present and discuss the available literature on the role of SIRT3 in cardiac physiology and disease. Frontiers Media S.A. 2016-10-13 /pmc/articles/PMC5061741/ /pubmed/27790619 http://dx.doi.org/10.3389/fcvm.2016.00038 Text en Copyright © 2016 Koentges, Bode and Bugger. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
repository_type	Open Access Journal
institution_category	Foreign Institution
institution	US National Center for Biotechnology Information
building	NCBI PubMed
collection	Online Access
language	English
format	Online
author	Koentges, Christoph Bode, Christoph Bugger, Heiko
spellingShingle	Koentges, Christoph Bode, Christoph Bugger, Heiko SIRT3 in Cardiac Physiology and Disease
author_facet	Koentges, Christoph Bode, Christoph Bugger, Heiko
author_sort	Koentges, Christoph
title	SIRT3 in Cardiac Physiology and Disease
title_short	SIRT3 in Cardiac Physiology and Disease
title_full	SIRT3 in Cardiac Physiology and Disease
title_fullStr	SIRT3 in Cardiac Physiology and Disease
title_full_unstemmed	SIRT3 in Cardiac Physiology and Disease
title_sort	sirt3 in cardiac physiology and disease
description	Functional defects in mitochondrial biology causally contribute to various human diseases, including cardiovascular disease. Impairment in oxidative phosphorylation, mitochondrial oxidative stress, and increased opening of the mitochondrial permeability transition pore add to the underlying mechanisms of heart failure or myocardial ischemia–reperfusion (IR) injury. Recent evidence demonstrated that the mitochondrial NAD+-dependent deacetylase sirtuin 3 (SIRT3) may regulate these mitochondrial functions by reversible protein lysine deacetylation. Loss of function studies demonstrated a role of impaired SIRT3 activity in the pathogenesis of myocardial IR injury as well as in the development of cardiac hypertrophy and the transition into heart failure. Gain of function studies and treatment approaches increasing mitochondrial NAD+ availability that ameliorate these cardiac pathologies have led to the proposal that activation of SIRT3 may represent a promising therapeutic strategy to improve mitochondrial derangements in various cardiac pathologies. In the current review, we will present and discuss the available literature on the role of SIRT3 in cardiac physiology and disease.
publisher	Frontiers Media S.A.
publishDate	2016
url	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5061741/
_version_	1613681831303970816

SIRT3 in Cardiac Physiology and Disease

Similar Items