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dc.contributor.authorNuche, Jorge 
dc.contributor.authorPalomino-Doza, Julián
dc.contributor.authorYnsaurriaga, Fernando Arribas
dc.contributor.authorDelgado, Juan F
dc.contributor.authorIbanez, Borja 
dc.contributor.authorOliver, Eduardo 
dc.contributor.authorSubías, Pilar Escribano
dc.date.accessioned2020-04-16T10:43:29Z
dc.date.available2020-04-16T10:43:29Z
dc.date.issued2020-04-04
dc.identifier.citationInt J Mol Sci. 2020; 21(7):2509es_ES
dc.identifier.issn1422-0067es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/9583
dc.description.abstractPulmonary arterial hypertension (PAH) is a rare disease caused by pulmonary vascular remodeling. Current vasodilator treatments have substantially improved patients' survival. This improved survival has led to the appearance of complications related to conditions previously underdiagnosed or even ignored, such as pulmonary artery aneurysm (PAA). The presence of a dilated pulmonary artery has been shown to be related to an increased risk of sudden cardiac death among PAH patients. This increased risk could be associated to the development of left main coronary artery compression or pulmonary artery dissection. Nevertheless, very little is currently known about the molecular mechanisms related to PAA. Thoracic aortic aneurysm (TAA) is a well-known condition with an increased risk of sudden death caused by acute aortic dissection. TAA may be secondary to chronic exposure to classic cardiovascular risk factors. In addition, a number of genetic variants have been shown to be related to a marked risk of TAA and dissection as part of multisystemic syndromes or isolated familial TAA. The molecular pathways implied in the development of TAA have been widely studied and described. Many of these molecular pathways are involved in the pathogenesis of PAH and could be involved in PAA. This review aims to describe all these common pathways to open new research lines that could help lead to a better understanding of the pathophysiology of PAH and PAA and their clinical implications.es_ES
dc.description.sponsorshipJ.N. is a recipient of a predoctoral grant (Jordi Soler Soler) through CIBERCV. E.O. is a recipient of funds from Programa de Atracción de Talento (2017-T1/BMD-5185) of Comunidad de Madrid. P.E. is a recipient of a grant of the Spanish Ministry of Science and Universities for the study of molecular bases in pulmonary arterial hypertension (PI 18/01233). The CNIC is supported by the Instituto de Salud Carlos III (ISCIII), the Ministerio de Ciencia e Innovación, and the Pro CNIC Foundation, and is a Severo Ochoa Center of Excellence (SEV-2015-0505).es_ES
dc.language.isoenges_ES
dc.publisherMDPIes_ES
dc.relation.isversionofPublisher's versiones_ES
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subjectaortic aneurysmes_ES
dc.subjectgenees_ES
dc.subjectmolecular biologyes_ES
dc.subjectpulmonary arterial hypertensiones_ES
dc.subjectpulmonary artery aneurysmes_ES
dc.titlePotential Molecular Pathways Related to Pulmonary Artery Aneurysm Development: Lessons to Learn from the Aortaes_ES
dc.typeArtículoes_ES
dc.rights.licenseAtribución 4.0 Internacional*
dc.identifier.pubmedID32260370es_ES
dc.format.volume21es_ES
dc.format.number7es_ES
dc.format.page2509es_ES
dc.identifier.doi10.3390/ijms21072509es_ES
dc.contributor.funderComunidad de Madrid
dc.contributor.funderMinisterio de Ciencia, Innovación y Universidades (España)
dc.contributor.funderInstituto de Salud Carlos III - ISCIII
dc.contributor.funderCentro de Investigación Biomedica en Red - CIBER
dc.contributor.funderFundación ProCNIC
dc.description.peerreviewedes_ES
dc.identifier.e-issn1422-0067es_ES
dc.relation.publisherversionhttps://doi.org/10.3390/ijms21072509es_ES
dc.identifier.journalInternational journal of molecular scienceses_ES
dc.repisalud.orgCNICCNIC::Grupos de investigación::Laboratorio Traslacional para la Imagen y Terapia Cardiovasculares_ES
dc.repisalud.institucionCNICes_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 4.0 Internacional
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