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dc.contributor.authorMarín-Aguilar, Fabiola
dc.contributor.authorLechuga-Vieco, Ana V. 
dc.contributor.authorAlcocer-Gómez, Elísabet
dc.contributor.authorCastejón-Vega, Beatriz
dc.contributor.authorLucas, Javier 
dc.contributor.authorGarrido, Carlos 
dc.contributor.authorPeralta-Garcia, Alejandro
dc.contributor.authorPérez-Pulido, Antonio J
dc.contributor.authorVarela-López, Alfonso
dc.contributor.authorQuiles, José L
dc.contributor.authorRyffel, Bernhard
dc.contributor.authorFlores, Ignacio 
dc.contributor.authorBullón, Pedro
dc.contributor.authorRuiz-Cabello, Jesus 
dc.contributor.authorCordero, Mario D
dc.date.accessioned2020-03-25T11:56:36Z
dc.date.available2020-03-25T11:56:36Z
dc.date.issued2020-01
dc.identifier.citationAging Cell. 2020; 19(1):e13050es_ES
dc.identifier.issn1474-9718es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/9327
dc.description.abstractWhile NLRP3-inflammasome has been implicated in cardiovascular diseases, its role in physiological cardiac aging is largely unknown. During aging, many alterations occur in the organism, which are associated with progressive impairment of metabolic pathways related to insulin resistance, autophagy dysfunction, and inflammation. Here, we investigated the molecular mechanisms through which NLRP3 inhibition may attenuate cardiac aging. Ablation of NLRP3-inflammasome protected mice from age-related increased insulin sensitivity, reduced IGF-1 and leptin/adiponectin ratio levels, and reduced cardiac damage with protection of the prolongation of the age-dependent PR interval, which is associated with atrial fibrillation by cardiovascular aging and reduced telomere shortening. Furthermore, old NLRP3 KO mice showed an inhibition of the PI3K/AKT/mTOR pathway and autophagy improvement, compared with old wild mice and preserved Nampt-mediated NAD+ levels with increased SIRT1 protein expression. These findings suggest that suppression of NLRP3 prevented many age-associated changes in the heart, preserved cardiac function of aged mice and increased lifespan.es_ES
dc.description.sponsorshipAndalusian regional government; Consejería de Salud de la Junta de Andalucia, Grant/ Award Number: PI‐0036‐2014; Ministerio de economía y competitividad, Grant/Award Number: SAF2017‐84494‐C2‐1‐Res_ES
dc.language.isoenges_ES
dc.publisherWileyes_ES
dc.relation.isversionofPublisher's versiones_ES
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subjectNLRP3-inflammasomees_ES
dc.subjectautophagyes_ES
dc.subjectcardiac aginges_ES
dc.subjectlongevityes_ES
dc.subjectmorbidityes_ES
dc.subjectmortalityes_ES
dc.titleNLRP3 inflammasome suppression improves longevity and prevents cardiac aging in male micees_ES
dc.typeArtículoes_ES
dc.rights.licenseAtribución 4.0 Internacional*
dc.identifier.pubmedID31625260es_ES
dc.format.volume19es_ES
dc.format.number1es_ES
dc.format.pagee13050es_ES
dc.identifier.doi10.1111/acel.13050es_ES
dc.contributor.funderJunta de Andalucíaes_ES
dc.contributor.funderMinisterio de Economía y Competitividad (España)es_ES
dc.description.peerreviewedes_ES
dc.identifier.e-issn1474-9726es_ES
dc.relation.publisherversionhttps://doi.org/10.1111/acel.13050es_ES
dc.identifier.journalAging celles_ES
dc.repisalud.orgCNICCNIC::Grupos de investigación::Regeneración y envejecimientoes_ES
dc.repisalud.orgCNICCNIC::Grupos de investigación::Genética Funcional del Sistema de Fosforilación Oxidativaes_ES
dc.repisalud.institucionCNICes_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/SAF2017‐84494‐C2‐1‐Res_ES
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses_ES


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