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dc.contributor.authorHamczyk, Magda R. 
dc.contributor.authordel Campo, Lara 
dc.contributor.authorAndres, Vicente 
dc.date.accessioned2019-07-19T12:44:09Z
dc.date.available2019-07-19T12:44:09Z
dc.date.issued2018-02
dc.identifier.citationAnnu Rev Physiol. 2018; 80:27-48es_ES
dc.identifier.issn0066-4278es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/7966
dc.description.abstractAging, the main risk factor for cardiovascular disease (CVD), is becoming progressively more prevalent in our societies. A better understanding of how aging promotes CVD is therefore urgently needed to develop new strategies to reduce disease burden. Atherosclerosis and heart failure contribute significantly to age-associated CVD-related morbimortality. CVD and aging are both accelerated in patients suffering from Hutchinson-Gilford progeria syndrome (HGPS), a rare genetic disorder caused by the prelamin A mutant progerin. Progerin causes extensive atherosclerosis and cardiac electrophysiological alterations that invariably lead to premature aging and death. This review summarizes the main structural and functional alterations to the cardiovascular system during physiological and premature aging and discusses the mechanisms underlying exaggerated CVD and aging induced by prelamin A and progerin. Because both proteins are expressed in normally aging non-HGPS individuals, and most hallmarks of normal aging occur in progeria, research on HGPS can identify mechanisms underlying physiological aging.es_ES
dc.description.sponsorshipProgeria Research Foundation (Established Investigator Award 2014-52). L.d.C. is the recipient of a Jordi Soler postdoctoral fellowship from the Red de Investigacion Cardiovascular at ISCIII. The CNIC is supported by the MEIC and the Pro-CNIC Foundation and is a Severo Ochoa Center of Excellence (MEIC award SEV-2015-0505).es_ES
dc.language.isoenges_ES
dc.type.hasVersionSMURes_ES
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.subjectAtherosclerosises_ES
dc.subjectCardiovascular diseasees_ES
dc.subjectHeart failurees_ES
dc.subjectPrelamin A/lamin Aes_ES
dc.subjectProgerines_ES
dc.subjectVascular calcificationes_ES
dc.subject.meshAging es_ES
dc.subject.meshAnimals es_ES
dc.subject.meshCardiovascular Diseases es_ES
dc.subject.meshCardiovascular System es_ES
dc.subject.meshHumans es_ES
dc.subject.meshProgeria es_ES
dc.subject.meshVascular Calcification es_ES
dc.titleAging in the Cardiovascular System: Lessons from Hutchinson-Gilford Progeria Syndromees_ES
dc.typejournal articlees_ES
dc.rights.licenseAtribución-NoComercial-CompartirIgual 4.0 Internacional*
dc.identifier.pubmedID28934587es_ES
dc.format.volume80es_ES
dc.format.number1es_ES
dc.format.page27-48es_ES
dc.identifier.doi10.1146/annurev-physiol-021317-121454es_ES
dc.contributor.funderProgeria Research Foundation 
dc.contributor.funderInstituto de Salud Carlos III 
dc.contributor.funderMinisterio de Economía, Industria y Competitividad (España) 
dc.contributor.funderFundación ProCNIC 
dc.identifier.e-issn1545-1585es_ES
dc.relation.publisherversionhttps://doi.org/10.1146/annurev-physiol-021317-121454es_ES
dc.identifier.journalAnnual review of physiologyes_ES
dc.repisalud.orgCNICCNIC::Grupos de investigación::Fisiopatología Cardiovascular Molecular y Genéticaes_ES
dc.repisalud.institucionCNICes_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/SEV-2015-0505es_ES
dc.rights.accessRightsopen accesses_ES


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Atribución-NoComercial-CompartirIgual 4.0 Internacional
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