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dc.contributor.authorAndres, Vicente 
dc.date.accessioned2019-07-17T06:16:34Z
dc.date.available2019-07-17T06:16:34Z
dc.date.issued2014-10
dc.identifier.citationAtherosclerosis. 2014; 236(2):444-447es_ES
dc.identifier.issn0021-9150es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/7916
dc.description.abstractSignaling via both vitamin D (VitD) and the renin-angiotensin system (RAS) plays important roles in physiological processes. Evidence has mounted linking cardiovascular disease to both increased activity of the RAS and VitD deficiency. Although several studies have established functional relationships between the RAS and VitD, many aspects of their complex interaction remain unknown. In this issue of Atherosclerosis, Valcheva and colleagues show that defective VitD signaling can promote vascular damage by inducing premature senescence of smooth muscle cells due to elevated local production of angiotensin II and reactive oxygen species, and upregulation of the tumor suppressor p57(Kip2).es_ES
dc.description.sponsorshipWork in the author's laboratory is supported by grants from the Ministerio de Economía y Competitividad (MINECO) and Fondo Europeo de Desarrollo Regional (FEDER) (grant No. SAF2013-46663-R), Instituto de Salud Carlos III (grant No. RD12/0042/0028), European Union FP7 (Liphos, grant No. 317916), and The Progeria Research Foundation (Innovator Award 2012, and Established Investigator Award 2014). The CNIC is supported by the MINECO and Pro-CNIC Foundation.es_ES
dc.language.isoenges_ES
dc.relation.isversionofPostprintes_ES
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectAngiotensines_ES
dc.subjectCell senescencees_ES
dc.subjectVascular smooth muscle celles_ES
dc.subjectVitamin Des_ES
dc.subjectp57es_ES
dc.subject.meshAnimals es_ES
dc.subject.meshCellular Senescence es_ES
dc.subject.meshFemale es_ES
dc.subject.meshMale es_ES
dc.subject.meshMuscle, Smooth, Vasculares_ES
dc.subject.meshReceptors, Calcitrioles_ES
dc.subject.meshVitamin D es_ES
dc.titleVitamin D puts the brakes on angiotensin II-induced oxidative stress and vascular smooth muscle cell senescencees_ES
dc.typeArtículoes_ES
dc.rights.licenseAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.identifier.pubmedID25173069es_ES
dc.format.volume236es_ES
dc.format.number2es_ES
dc.format.page444-7es_ES
dc.identifier.doi10.1016/j.atherosclerosis.2014.07.031es_ES
dc.contributor.funderMinisterio de Economía y Competitividad (España)
dc.contributor.funderInstituto de Salud Carlos III - ISCIII
dc.contributor.funderEuropean Regional Development Fund (ERDF/FEDER)
dc.contributor.funderEuropean Commission
dc.contributor.funderProgeria Research Foundation
dc.contributor.funderFundación ProCNIC
dc.identifier.e-issn1879-1484es_ES
dc.identifier.journalAtherosclerosises_ES
dc.repisalud.orgCNICCNIC::Grupos de investigación::Fisiopatología Cardiovascular Molecular y Genéticaes_ES
dc.repisalud.institucionCNICes_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/SAF2013-46663-Res_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/RD12/0042/0028es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/EC/FP7/317916/EUes_ES
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses_ES


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Attribution-NonCommercial-NoDerivatives 4.0 Internacional
This item is licensed under a: Attribution-NonCommercial-NoDerivatives 4.0 Internacional