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Authordc.contributor.authorSánchez, Gina 
Authordc.contributor.authorAraneda, Felipe 
Authordc.contributor.authorPeña, Juan Pedro 
Authordc.contributor.authorFinkelstein, José Pablo 
Authordc.contributor.authorRiquelme, Jaime A. 
Authordc.contributor.authorMontecinos, Luis 
Authordc.contributor.authorBarrientos Briones, Genaro 
Authordc.contributor.authorLlanos Vidal, Paola 
Authordc.contributor.authorPedrozo Cibils, Zully 
Authordc.contributor.authorSaid, Matilde 
Authordc.contributor.authorBull Simpfendorfer, Ricardo 
Authordc.contributor.authorDonoso Laurent, Paulina 
Admission datedc.date.accessioned2018-07-19T22:21:46Z
Available datedc.date.available2018-07-19T22:21:46Z
Publication datedc.date.issued2018
Cita de ítemdc.identifier.citationInt. J. Mol. Sci. 2018, 19, 533es_ES
Identifierdc.identifier.other10.3390/ijms19020533
Identifierdc.identifier.urihttp://repositorio.uchile.cl/handle/2250/150031
Abstractdc.description.abstractVentricular arrhythmias are a common cause of sudden cardiac death, and their occurrence is higher in obese subjects. Abnormal gating of ryanodine receptors (RyR2), the calcium release channels of the sarcoplasmic reticulum, can produce ventricular arrhythmias. Since obesity promotes oxidative stress and RyR2 are redox-sensitive channels, we investigated whether the RyR2 activity was altered in obese mice. Mice fed a high fat diet (HFD) became obese after eight weeks and exhibited a significant increase in the occurrence of ventricular arrhythmias. Single RyR2 channels isolated from the hearts of obese mice were more active in planar bilayers than those isolated from the hearts of the control mice. At the molecular level, RyR2 channels from HFD-fed mice had substantially fewer free thiol residues, suggesting that redox modifications were responsible for the higher activity. Apocynin, provided in the drinking water, completely prevented the appearance of ventricular arrhythmias in HFD-fed mice, and normalized the activity and content of the free thiol residues of the protein. HFD increased the expression of NOX4, an isoform of NADPH oxidase, in the heart. Our results suggest that HFD increases the activity of RyR2 channels via a redox-dependent mechanism, favoring the appearance of ventricular arrhythmias.es_ES
Patrocinadordc.description.sponsorshipFondo Nacional de Investigacion Cientifica y Tecnologica, Chile (Fondecyt) 1160704 11150243 3160298 1150887 Agencia Nacional de Promocion Cientifica y Tecnologica, Argentina PICT 0856es_ES
Lenguagedc.language.isoenes_ES
Publisherdc.publisherMDPIes_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.sourceInternational Journal of Molecular Scienceses_ES
Keywordsdc.subjectCalcium release channelses_ES
Keywordsdc.subjectReactive oxygen species (ROS)es_ES
Keywordsdc.subjectRedox modificationses_ES
Keywordsdc.subjectVentricular tachycardiaes_ES
Keywordsdc.subjectNADPH oxidasees_ES
Títulodc.titleHigh fat diet induced obesity produces spontaneous ventricular arrhythmias and increases the activity of ryanodine receptors in micees_ES
Document typedc.typeArtículo de revistaes_ES
Catalogueruchile.catalogadortjnes_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