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dc.contributor.authorDorado, Beatriz 
dc.contributor.authorAndres, Vicente 
dc.date.accessioned2019-07-19T08:47:19Z
dc.date.available2019-07-19T08:47:19Z
dc.date.issued2017
dc.identifier.citationCurr Opin Cell Biol. 2017; 46:17-25es_ES
dc.identifier.issn0955-0674es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/7959
dc.description.abstractLamin A is a nuclear intermediate filament protein with important structural and regulatory roles in most differentiated mammalian cells. Excessive accumulation of its precursor prelamin A or the mutant form called 'progerin' causes premature aging syndromes. Progeroid 'laminopathies' are characterized by severe cardiovascular problems (cardiac electrical defects, vascular calcification and stiffening, atherosclerosis, myocardial infarction, and stroke) and premature death. Here, we review studies in cell and mouse models and patients that are unraveling how abnormal prelamin A and progerin accumulation accelerates cardiovascular disease and aging. This knowledge is essential for developing effective therapies to treat progeria and may help identify new mechanisms underlying normal aging.es_ES
dc.description.sponsorshipWork in the laboratory of V.A. is supported by the Spanish Ministerio de Economia, Industria y Competitividad (MINECO) (SAF2013-46663-R) and the Instituto de Salud Carlos III (RD12/0042/0028) with co-funding from the Fondo Europeo de Desarrollo Regional (FEDER), the Fundacio Marato TV3 (122/C/2015), and the Progeria Research Foundation (Established Investigator Award 2014-52). The CNIC is supported by the MINECO and the Pro-CNIC Foundation, and is a Severo Ochoa Center of Excellence (MINECO award SEV-2015-0505).es_ES
dc.language.isoenges_ES
dc.relation.isversionofPostprintes_ES
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.subject.meshAging es_ES
dc.subject.meshAnimals es_ES
dc.subject.meshCardiovascular Diseases es_ES
dc.subject.meshCell Nucleus es_ES
dc.subject.meshDisease Models, Animales_ES
dc.subject.meshHumans es_ES
dc.subject.meshLamin Type A es_ES
dc.subject.meshProgeria es_ES
dc.titleA-type lamins and cardiovascular disease in premature aging syndromeses_ES
dc.typeArtículoes_ES
dc.rights.licenseAtribución-NoComercial-CompartirIgual 4.0 Internacional*
dc.identifier.pubmedID28086161es_ES
dc.format.volume46es_ES
dc.format.page17-25es_ES
dc.identifier.doi10.1016/j.ceb.2016.12.005es_ES
dc.contributor.funderMinisterio de Economía, Industria y Competitividad (España)
dc.contributor.funderInstituto de Salud Carlos III - ISCIII
dc.contributor.funderEuropean Regional Development Fund (ERDF/FEDER)
dc.contributor.funderFundacio La Marato
dc.contributor.funderProgeria Research Foundation
dc.contributor.funderFundación ProCNIC
dc.description.peerreviewedes_ES
dc.identifier.e-issn1879-0410es_ES
dc.relation.publisherversionhttps://doi.org/10.1016/j.ceb.2016.12.005es_ES
dc.identifier.journalCurrent opinion in cell biologyes_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/ES/SEV-2015-0505es_ES
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses_ES


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Atribución-NoComercial-CompartirIgual 4.0 Internacional
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