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Author | dc.contributor.author | Gutiérrez, Tomás | |
Author | dc.contributor.author | Parra, Valentina | |
Author | dc.contributor.author | Troncoso, Rodrigo | |
Author | dc.contributor.author | Pennanen, Christian | |
Author | dc.contributor.author | Contreras Ferrat, Ariel Eduardo | |
Author | dc.contributor.author | Vásquez Trincado, César Alonso | |
Author | dc.contributor.author | Morales, Pablo E. | |
Author | dc.contributor.author | López Crisosto, Camila | |
Author | dc.contributor.author | Sotomayor Flores, Cristian Alejandro | |
Author | dc.contributor.author | Chiong Lay, Mario | |
Author | dc.contributor.author | Rothermel, Beverly A. | |
Author | dc.contributor.author | Lavandero González, Sergio | |
Admission date | dc.date.accessioned | 2018-12-20T15:13:15Z | |
Available date | dc.date.available | 2018-12-20T15:13:15Z | |
Publication date | dc.date.issued | 2014 | |
Cita de ítem | dc.identifier.citation | Cell Communication and Signaling, Volumen 12, Issue 1, 2018, | |
Identifier | dc.identifier.issn | 1478811X | |
Identifier | dc.identifier.other | 10.1186/s12964-014-0068-4 | |
Identifier | dc.identifier.uri | https://repositorio.uchile.cl/handle/2250/158560 | |
Abstract | dc.description.abstract | © 2014 Gutierrez et al.; licensee BioMed Central Ltd. Background: Cardiac hypertrophy is characterized by alterations in both cardiac bioenergetics and insulin sensitivity. Insulin promotes glucose uptake by cardiomyocytes and its use as a substrate for glycolysis and mitochondrial oxidation in order to maintain the high cardiac energy demands. Insulin stimulates Ca2+ release from the endoplasmic reticulum, however, how this translates to changes in mitochondrial metabolism in either healthy or hypertrophic cardiomyocytes is not fully understood. Results: In the present study we investigated insulin-dependent mitochondrial Ca2+ signaling in normal and norepinephrine or insulin like growth factor-1-induced hypertrophic cardiomyocytes. Using mitochondrion-selective Ca2+-fluorescent probes we showed that insulin increases mitochondrial Ca2+ levels. This signal was inhibited by the pharmacological blockade of either the inositol 1,4,5-triphosphate receptor or the mitochondrial Ca2+ uniport | |
Lenguage | dc.language.iso | en | |
Publisher | dc.publisher | BioMed Central Ltd. | |
Type of license | dc.rights | Attribution-NonCommercial-NoDerivs 3.0 Chile | |
Link to License | dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/3.0/cl/ | |
Source | dc.source | Cell Communication and Signaling | |
Keywords | dc.subject | Akt | |
Keywords | dc.subject | Calcium | |
Keywords | dc.subject | Cardiac hypertrophy | |
Keywords | dc.subject | Catecholamines | |
Keywords | dc.subject | IGF-1 | |
Keywords | dc.subject | Inositol 1,4,5-triphosphate receptor | |
Keywords | dc.subject | Insulin | |
Keywords | dc.subject | Mitochondria | |
Título | dc.title | Alteration in mitochondrial Ca2+ uptake disrupts insulin signaling in hypertrophic cardiomyocytes | |
Document type | dc.type | Artículo de revista | |
dcterms.accessRights | dcterms.accessRights | Acceso Abierto | |
Cataloguer | uchile.catalogador | SCOPUS | |
Indexation | uchile.index | Artículo de publicación SCOPUS | |
uchile.cosecha | uchile.cosecha | SI | |
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