Cardiomyocyte death: Mechanisms and translational implications

M. Chiong; Z. V. Wang; Z. Pedrozo; D. J. Cao; R. Troncoso; M. Ibacache; A. Criollo; A. Nemchenko; J. A. Hill; S. Lavandero

doi:10.1038/cddis.2011.130

Cardiomyocyte death: Mechanisms and translational implications

M. Chiong, Z. V. Wang, Z. Pedrozo, D. J. Cao, R. Troncoso, M. Ibacache, A. Criollo, A. Nemchenko, J. A. Hill, S. Lavandero

Universidad de Chile

Résultat de recherche › examen par les pairs

380 Citations (Scopus)

Résumé

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.

Langue d'origine	English
Numéro d'article	e244
Journal	Cell Death and Disease
Volume	2
Numéro de publication	12
DOI	https://doi.org/10.1038/cddis.2011.130
Statut de publication	Published - déc. 2011

Financement

Acknowledgements. We thank the members from the Hill lab and Lavandero lab for helpful discussions. This work was supported by grants from the NIH (HL-075173, JAH; HL-080144, JAH; and HL-090842, JAH), AHA (0640084N, JAH), the AHA-Jon Holden DeHaan Foundation (0970518N, JAH), and the Fondo Nacional de Desarrollo Cientifico y Tecnologico: FONDECYT 1080436 and FONDAP 15010006 (SL). ZVW, ZP, and RT are supported by postdoctoral fellowships from the American Heart Association 10POST4320009 and FONDECYT 3110039 and 3110114, respectively.

Bailleurs de fonds	Numéro du bailleur de fonds
AHA-Jon Holden DeHaan Foundation	0970518N
National Institutes of Health	HL-075173, HL-090842
National Heart, Lung, and Blood Institute	R01HL080144
American Heart Association	3110114, 10POST4320009, 0640084N, 3110039
Fondo Nacional de Desarrollo Científico y Tecnológico	1080436, FONDAP 15010006

ASJC Scopus Subject Areas

Immunology
Cellular and Molecular Neuroscience
Cell Biology
Cancer Research

ODD de l’ONU

Cette action contribue à la réalisation des objectifs de développement durable suivants

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10.1038/cddis.2011.130

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abstract = "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.",

author = "M. Chiong and Wang, {Z. V.} and Z. Pedrozo and Cao, {D. J.} and R. Troncoso and M. Ibacache and A. Criollo and A. Nemchenko and Hill, {J. A.} and S. Lavandero",

note = "Funding Information: Acknowledgements. We thank the members from the Hill lab and Lavandero lab for helpful discussions. This work was supported by grants from the NIH (HL-075173, JAH; HL-080144, JAH; and HL-090842, JAH), AHA (0640084N, JAH), the AHA-Jon Holden DeHaan Foundation (0970518N, JAH), and the Fondo Nacional de Desarrollo Cientifico y Tecnologico: FONDECYT 1080436 and FONDAP 15010006 (SL). ZVW, ZP, and RT are supported by postdoctoral fellowships from the American Heart Association 10POST4320009 and FONDECYT 3110039 and 3110114, respectively.",

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doi = "10.1038/cddis.2011.130",

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AU - Chiong, M.

AU - Wang, Z. V.

AU - Pedrozo, Z.

AU - Cao, D. J.

AU - Troncoso, R.

AU - Ibacache, M.

AU - Criollo, A.

AU - Nemchenko, A.

AU - Hill, J. A.

AU - Lavandero, S.

N1 - Funding Information: Acknowledgements. We thank the members from the Hill lab and Lavandero lab for helpful discussions. This work was supported by grants from the NIH (HL-075173, JAH; HL-080144, JAH; and HL-090842, JAH), AHA (0640084N, JAH), the AHA-Jon Holden DeHaan Foundation (0970518N, JAH), and the Fondo Nacional de Desarrollo Cientifico y Tecnologico: FONDECYT 1080436 and FONDAP 15010006 (SL). ZVW, ZP, and RT are supported by postdoctoral fellowships from the American Heart Association 10POST4320009 and FONDECYT 3110039 and 3110114, respectively.

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AB - 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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Cardiomyocyte death: Mechanisms and translational implications

Résumé

Financement

ASJC Scopus Subject Areas

ODD de l’ONU

Accès au document

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