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Authordc.contributor.authorFerdous, Anwarul 
Authordc.contributor.authorWang, Zhao V. 
Authordc.contributor.authorLuo, Yuxuan 
Authordc.contributor.authorLi, Dan L. 
Authordc.contributor.authorLuo, Xiang 
Authordc.contributor.authorSchiattarella, Gabriele G. 
Authordc.contributor.authorAltamirano, Francisco 
Authordc.contributor.authorMay, Herman I. 
Authordc.contributor.authorBattiprolu, Pavan K. 
Authordc.contributor.authorNguyen, Annie 
Authordc.contributor.authorRothermel, Beverly A. 
Authordc.contributor.authorLavandero González, Sergio 
Authordc.contributor.authorGillette, Thomas G. 
Authordc.contributor.authorHill, Joseph A. 
Admission datedc.date.accessioned2020-06-24T00:13:28Z
Available datedc.date.available2020-06-24T00:13:28Z
Publication datedc.date.issued2020
Cita de ítemdc.identifier.citationNature Communications Volumen: 11 Número: 1 May 21 2020es_ES
Identifierdc.identifier.other10.1038/s41467-020-16345-y
Identifierdc.identifier.urihttp://repositorio.uchile.cl/handle/2250/175667
Abstractdc.description.abstractForkhead box O (FoxO) proteins and thyroid hormone (TH) have well established roles in cardiovascular morphogenesis and remodeling. However, specific role(s) of individual FoxO family members in stress-induced growth and remodeling of cardiomyocytes remains unknown. Here, we report that FoxO1, but not FoxO3, activity is essential for reciprocal regulation of types II and III iodothyronine deiodinases (Dio2 and Dio3, respectively), key enzymes involved in intracellular TH metabolism. We further show that Dio2 is a direct transcriptional target of FoxO1, and the FoxO1-Dio2 axis governs TH-induced hypertrophic growth of neonatal cardiomyocytes in vitro and in vivo. Utilizing transverse aortic constriction as a model of hemodynamic stress in wild-type and cardiomyocyte-restricted FoxO1 knockout mice, we unveil an essential role for the FoxO1-Dio2 axis in afterload-induced pathological cardiac remodeling and activation of TR alpha 1. These findings demonstrate a previously unrecognized FoxO1-Dio2 signaling axis in stress-induced cardiomyocyte growth and remodeling and intracellular TH homeostasis. Disease stress-induced cardiac hypertrophy is a major mechanism of pathological cardiac remodeling. Here, the authors unveil a previously unrecognized role of a FoxO1-Dio2 signaling axis in maladaptive, afterload-induced cardiac hypertrophy and intracellular thyroid hormone homeostasis.es_ES
Patrocinadordc.description.sponsorshipUnited States Department of Health & Human Services National Institutes of Health (NIH) - USA HL-120732 HL-128215 HL-126012 HL-147933 HD-101006 HD-087351 American Heart Association 14SFRN20740000 19TPA34920001 19CDA34680003 18POST34060230 CPRIT RP110486P3 Leducq Foundation 11CVD04 Comision Nacional de Investigacion Cientifica y Tecnologica de Chile Fondo de Financiamiento de Centros de Investigacion en Areas Prioritarias (FONDAP) 15130011 Comision Nacional de Investigacion Cientifica y Tecnologica (CONICYT) CONICYT FONDECYT 1161156 Scientist Development Grant (SDG) from the AHA 14SDG18440002 American Heart Association 14PRE19770000es_ES
Lenguagedc.language.isoenes_ES
Publisherdc.publisherNaturees_ES
Type of licensedc.rightsAttribution-NonCommercial-NoDerivs 3.0 Chile*
Link to Licensedc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/cl/*
Sourcedc.sourceNature Communicationses_ES
Keywordsdc.subjectFoxo transcription factorses_ES
Keywordsdc.subjectCardiac-Hypertrophyes_ES
Keywordsdc.subjectGene-expressiones_ES
Keywordsdc.subjectProteines_ES
Keywordsdc.subjectHeartes_ES
Keywordsdc.subjectDeiodinasees_ES
Keywordsdc.subjectDeacetylationes_ES
Keywordsdc.subjectType-2es_ES
Keywordsdc.subjectRegenerationes_ES
Keywordsdc.subjectSuppressiones_ES
Títulodc.titleFoxO1-Dio2 signaling axis governs cardiomyocyte thyroid hormone metabolism and hypertrophic growthes_ES
Document typedc.typeArtículo de revistaes_ES
Catalogueruchile.catalogadorlajes_ES
Indexationuchile.indexArtículo de publicación ISIes_ES


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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