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Authordc.contributor.authorZepeda Iriarte, Ramiro 
Authordc.contributor.authorKuzmicic, Jovan 
Authordc.contributor.authorParra Ortiz, Valentina 
Authordc.contributor.authorTroncoso Cotal, Rodrigo 
Authordc.contributor.authorPennanen, Christian 
Authordc.contributor.authorRiquelme, Jaime A. 
Authordc.contributor.authorPedrozo Cibils, Zully 
Authordc.contributor.authorChiong Lay, Mario 
Authordc.contributor.authorSánchez, Gina 
Authordc.contributor.authorLavandero González, Sergio 
Admission datedc.date.accessioned2019-01-29T13:56:17Z
Available datedc.date.available2019-01-29T13:56:17Z
Publication datedc.date.issued2014
Cita de ítemdc.identifier.citationJ Cardiovasc Pharmacol! 2014;63:477–487
Identifierdc.identifier.issn15334023
Identifierdc.identifier.issn01602446
Identifierdc.identifier.other10.1097/FJC.0000000000000071
Identifierdc.identifier.urihttp://repositorio.uchile.cl/handle/2250/160118
Abstractdc.description.abstractMitochondria are key organelles for ATP production in cardiomyocytes, which is regulated by processes of fission and fusion. We hypothesized that the mitochondria fusion protein dynamin-related protein 1 (Drp1) inhibition, attenuates ischemia-reperfusion (I/R) injury through modifications in mitochondrial metabolism. Rats were subjected to I/R through coronary artery ligation, and isolated cardiomyocytes were treated with an ischemia-mimicking solution. In vivo, cardiac function, myocardial infarction area, and mitochondrial morphology were determined, whereas in vitro, viability, mitochondrial membrane potential, intracellular ATP levels, and oxygen consumption rate (OCR) were assessed. In both models, an adenovirus expressing Drp1 dominant-negative K38A (Drp1K38A) was used to induce Drp1 loss-of-function. Our results showed that I/R stimulated mitochondrial fission. Myocardial infarction size and cell death induced by I/R were significantly reduced, whereas cardiac function after I/R
Lenguagedc.language.isoen
Publisherdc.publisherLippincott Williams and Wilkins
Type of licensedc.rightsAttribution-NonCommercial-NoDerivs 3.0 Chile
Link to Licensedc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/cl/
Sourcedc.sourceJournal of Cardiovascular Pharmacology
Keywordsdc.subjectDrp1
Keywordsdc.subjectIschemia/reperfusion
Keywordsdc.subjectMetabolism
Keywordsdc.subjectMitochondria
Keywordsdc.subjectMitochondrial fission
Títulodc.titleDrp1 loss-of-function reduces cardiomyocyte oxygen dependence protecting the heart from ischemia-reperfusion injury
Document typedc.typeArtículo de revista
Catalogueruchile.catalogadorlaj
Indexationuchile.indexArtículo de publicación SCOPUS
uchile.cosechauchile.cosechaSI


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Attribution-NonCommercial-NoDerivs 3.0 Chile
Except where otherwise noted, this item's license is described as Attribution-NonCommercial-NoDerivs 3.0 Chile