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dc.contributor.authorde Yébenes, Virginia G 
dc.contributor.authorBriones, Ana M
dc.contributor.authorMartos-Folgado, Inmaculada
dc.contributor.authorMur, Sonia M. 
dc.contributor.authorOller, Jorge 
dc.contributor.authorBilal, Faiz
dc.contributor.authorGonzález-Amor, María
dc.contributor.authorMendez-Barbero, Nerea 
dc.contributor.authorSilla-Castro, Juan Carlos 
dc.contributor.authorWere, Felipe 
dc.contributor.authorJimenez-Borreguero, Luis J 
dc.contributor.authorSanchez-Cabo, Fatima 
dc.contributor.authorBueno, Héctor 
dc.contributor.authorSalaices, Mercedes
dc.contributor.authorRedondo, Juan Miguel 
dc.contributor.authorRamiro, Almudena R 
dc.date.accessioned2021-06-23T07:41:28Z
dc.date.available2021-06-23T07:41:28Z
dc.date.issued2020-10
dc.identifier.citationArterioscler Thromb Vasc Biol. 2020; 40(10):2408-2424es_ES
dc.identifier.issn1524-4636es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/13177
dc.description.abstractmicroRNAs are master regulators of gene expression with essential roles in virtually all biological processes. miR-217 has been associated with aging and cellular senescence, but its role in vascular disease is not understood. Approach and Results: We have used an inducible endothelium-specific knock-in mouse model to address the role of miR-217 in vascular function and atherosclerosis. miR-217 reduced NO production and promoted endothelial dysfunction, increased blood pressure, and exacerbated atherosclerosis in proatherogenic apoE-/- mice. Moreover, increased endothelial miR-217 expression led to the development of coronary artery disease and altered left ventricular heart function, inducing diastolic and systolic dysfunction. Conversely, inhibition of endogenous vascular miR-217 in apoE-/- mice improved vascular contractility and diminished atherosclerosis. Transcriptome analysis revealed that miR-217 regulates an endothelial signaling hub and downregulates a network of eNOS (endothelial NO synthase) activators, including VEGF (vascular endothelial growth factor) and apelin receptor pathways, resulting in diminished eNOS expression. Further analysis revealed that human plasma miR-217 is a biomarker of vascular aging and cardiovascular risk. Our results highlight the therapeutic potential of miR-217 inhibitors in aging-related cardiovascular disease.es_ES
dc.description.sponsorshipV.G. de Yébenes was supported by Ramón y Cajal grant RYC-2009-04503 and AECC foundation grant INVES18013GARC and by the Universidad Complutense de Madrid. S.M. Mur and A.R. Ramiro are supported by Centro Nacional de Investigaciones Cardiovasculares (CNIC) funding. A.R. Ramiro was supported by the Spanish Ministerio de Ciencia e Innovación (PID2019-107551RB-I00), the Spanish Ministerio de Economía, Industria y Competitividad (SAF2013-42767-R and SAF2016-75511-R), and the European Research Council StG BCLYM. M. Salaices was supported by the Ministerio de Ciencia e Innovación (SAF2016-80305P) and with J. Miguel Redondo by Instituto de Salud Carlos III (CIBER de Enfermedades Cardiovasculares, CB16/11/00286 and CB16/11/00264) and Comunidad de Madrid (B2017/BMD-3676). V.G. de Yébenes was supported by Ministerio de Ciencia e Innovación (PID2019-107551RB-I00). Further support was provided by the European Social Fund and the European Regional Development Fund “A Way to Build Europe.” The CNIC is supported by Ministerio de Ciencia, Innovacion y Universidades, and the Pro CNIC Foundation and is a Severo Ochoa Center of Excellence (SEV-2015-0505).es_ES
dc.language.isoenges_ES
dc.publisherLippincott, Williams & Wilkinses_ES
dc.relation.isversionofPublisher's versiones_ES
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subject.meshPlaque, Atherosclerotices_ES
dc.subject.meshAge Factors es_ES
dc.subject.meshAged, 80 and over es_ES
dc.subject.meshAging es_ES
dc.subject.meshAnimals es_ES
dc.subject.meshAtherosclerosis es_ES
dc.subject.meshCase-Control Studies es_ES
dc.subject.meshCells, Cultured es_ES
dc.subject.meshCoronary Artery Disease es_ES
dc.subject.meshDisease Models, Animales_ES
dc.subject.meshEndothelial Cells es_ES
dc.subject.meshFemale es_ES
dc.subject.meshHemodynamics es_ES
dc.subject.meshHumans es_ES
dc.subject.meshMice, Inbred C57BL es_ES
dc.subject.meshMice, Knockout, ApoE es_ES
dc.subject.meshMicroRNAs es_ES
dc.subject.meshMiddle Aged es_ES
dc.subject.meshNitric Oxide es_ES
dc.subject.meshNitric Oxide Synthase Type III es_ES
dc.subject.meshSignal Transduction es_ES
dc.subject.meshVentricular Dysfunction, Left es_ES
dc.subject.meshVentricular Function, Left es_ES
dc.titleAging-Associated miR-217 Aggravates Atherosclerosis and Promotes Cardiovascular Dysfunction.es_ES
dc.typeArtículoes_ES
dc.rights.licenseAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.identifier.pubmedID32847388es_ES
dc.format.volume40es_ES
dc.format.number10es_ES
dc.format.page2408-2424es_ES
dc.identifier.doi10.1161/ATVBAHA.120.314333es_ES
dc.contributor.funderFundación Científica AECCes_ES
dc.contributor.funderUniversidad Complutense de Madrid (España)es_ES
dc.contributor.funderFundación ProCNICes_ES
dc.contributor.funderMinisterio de Ciencia e Innovación (España)es_ES
dc.contributor.funderMinisterio de Economía, Industria y Competitividad (España)es_ES
dc.contributor.funderEuropean Research Counciles_ES
dc.contributor.funderInstituto de Salud Carlos III - ISCIIIes_ES
dc.contributor.funderComunidad de Madrides_ES
dc.contributor.funderEuropean Regional Development Fund (ERDF/FEDER)es_ES
dc.description.peerreviewedes_ES
dc.relation.publisherversionhttps://doi.org/10.1161/ATVBAHA.120.314333es_ES
dc.identifier.journalArteriosclerosis, thrombosis, and vascular biologyes_ES
dc.repisalud.orgCNICCNIC::Grupos de investigación::Biología de linfocitos Bes_ES
dc.repisalud.orgCNICCNIC::Grupos de investigación::Investigación Cardiovascular Traslacional Multidisciplinariaes_ES
dc.repisalud.orgCNICCNIC::Grupos de investigación::Regulación Génica en Remodelado Vascular e Inflamaciónes_ES
dc.repisalud.orgCNICCNIC::Unidades técnicas::Bioinformáticaes_ES
dc.repisalud.institucionCNICes_ES
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses_ES
dc.relation.projectFECYTinfo:eu-repo/grantAgreement/ES/RYC-2009-04503es_ES
dc.relation.projectFECYTinfo:eu-repo/grantAgreement/ES/INVES18013GARCes_ES
dc.relation.projectFECYTinfo:eu-repo/grantAgreement/ES/PID2019-107551RB-I00es_ES
dc.relation.projectFECYTinfo:eu-repo/grantAgreement/ES/SAF2013-42767-Res_ES
dc.relation.projectFECYTinfo:eu-repo/grantAgreement/ES/SAF2016-75511-Res_ES
dc.relation.projectFECYTinfo:eu-repo/grantAgreement/ES/SAF2016-80305Pes_ES
dc.relation.projectFECYTinfo:eu-repo/grantAgreement/ES/CB16/11/00286es_ES
dc.relation.projectFECYTinfo:eu-repo/grantAgreement/ES/CB16/11/00264es_ES
dc.relation.projectFECYTinfo:eu-repo/grantAgreement/ES/B2017/BMD-3676es_ES
dc.relation.projectFECYTinfo:eu-repo/grantAgreement/ES/PID2019-107551RB-I00es_ES
dc.relation.projectFECYTinfo:eu-repo/grantAgreement/ES/SEV-2015-0505es_ES


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Attribution-NonCommercial-NoDerivatives 4.0 Internacional
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