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Cardiomyocyte death: mechanisms and translational implications

Cardiovascular disease (CVD) is the leading cause of morbidity and mortality worldwide. Although treatments have improved, development of novel therapies for patients with CVD remains a major research goal. Apoptosis, necrosis, and autophagy occur in cardiac myocytes, and both gradual and acute cell...

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Autores principales: Chiong, M, Wang, Z V, Pedrozo, Z, Cao, D J, Troncoso, R, Ibacache, M, Criollo, A, Nemchenko, A, Hill, J A, Lavandero, S
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3252742/
https://www.ncbi.nlm.nih.gov/pubmed/22190003
http://dx.doi.org/10.1038/cddis.2011.130
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author Chiong, M
Wang, Z V
Pedrozo, Z
Cao, D J
Troncoso, R
Ibacache, M
Criollo, A
Nemchenko, A
Hill, J A
Lavandero, S
author_facet Chiong, M
Wang, Z V
Pedrozo, Z
Cao, D J
Troncoso, R
Ibacache, M
Criollo, A
Nemchenko, A
Hill, J A
Lavandero, S
author_sort Chiong, M
collection PubMed
description Cardiovascular disease (CVD) is the leading cause of morbidity and mortality worldwide. Although treatments have improved, development of novel therapies for patients with CVD remains a major research goal. Apoptosis, necrosis, and autophagy occur in cardiac myocytes, and both gradual and acute cell death are hallmarks of cardiac pathology, including heart failure, myocardial infarction, and ischemia/reperfusion. Pharmacological and genetic inhibition of autophagy, apoptosis, or necrosis diminishes infarct size and improves cardiac function in these disorders. Here, we review recent progress in the fields of autophagy, apoptosis, and necrosis. In addition, we highlight the involvement of these mechanisms in cardiac pathology and discuss potential translational implications.
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spelling pubmed-32527422012-01-06 Cardiomyocyte death: mechanisms and translational implications Chiong, M Wang, Z V Pedrozo, Z Cao, D J Troncoso, R Ibacache, M Criollo, A Nemchenko, A Hill, J A Lavandero, S Cell Death Dis Review Cardiovascular disease (CVD) is the leading cause of morbidity and mortality worldwide. Although treatments have improved, development of novel therapies for patients with CVD remains a major research goal. Apoptosis, necrosis, and autophagy occur in cardiac myocytes, and both gradual and acute cell death are hallmarks of cardiac pathology, including heart failure, myocardial infarction, and ischemia/reperfusion. Pharmacological and genetic inhibition of autophagy, apoptosis, or necrosis diminishes infarct size and improves cardiac function in these disorders. Here, we review recent progress in the fields of autophagy, apoptosis, and necrosis. In addition, we highlight the involvement of these mechanisms in cardiac pathology and discuss potential translational implications. Nature Publishing Group 2011-12 2011-12-22 /pmc/articles/PMC3252742/ /pubmed/22190003 http://dx.doi.org/10.1038/cddis.2011.130 Text en Copyright © 2011 Macmillan Publishers Limited http://creativecommons.org/licenses/by-nc-nd/3.0/ This work is licensed under the Creative Commons Attribution-NonCommercial-No Derivative Works 3.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-nd/3.0/
spellingShingle Review
Chiong, M
Wang, Z V
Pedrozo, Z
Cao, D J
Troncoso, R
Ibacache, M
Criollo, A
Nemchenko, A
Hill, J A
Lavandero, S
Cardiomyocyte death: mechanisms and translational implications
title Cardiomyocyte death: mechanisms and translational implications
title_full Cardiomyocyte death: mechanisms and translational implications
title_fullStr Cardiomyocyte death: mechanisms and translational implications
title_full_unstemmed Cardiomyocyte death: mechanisms and translational implications
title_short Cardiomyocyte death: mechanisms and translational implications
title_sort cardiomyocyte death: mechanisms and translational implications
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3252742/
https://www.ncbi.nlm.nih.gov/pubmed/22190003
http://dx.doi.org/10.1038/cddis.2011.130
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