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dc.contributor.authorFuentes Q, Eduardo
dc.contributor.authorFuentes Q, Francisco
dc.contributor.authorAndres, Vicente 
dc.contributor.authorPello, Oscar M 
dc.contributor.authorFont de Mora, Jaime 
dc.contributor.authorPalomo G, Iván
dc.date.accessioned2019-06-07T12:54:07Z
dc.date.available2019-06-07T12:54:07Z
dc.date.issued2013
dc.identifier.citationPlatelets. 2013; 24(4):255-62es_ES
dc.identifier.issn0953-7104es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/7757
dc.description.abstractPlatelets, crucial mediators of the acute complications of atherosclerosis that cause life-threatening ischemic events at late stages of the disease, are also key effectors of inflammation throughout plaque development through their interaction with endothelial and immune cells in the injured vessel wall. During the first steps of atherosclerosis, blood inflammatory leukocytes interact with the damaged endothelium in areas rich in platelet aggregates. In late stages of the disease, platelets secrete several inflammatory molecules, even without forming aggregates. These molecules exacerbate the inflammation and induce the transition from chronic to acute disease, featuring increased instability of the atherosclerotic lesion that results in plaque rupture and thrombosis. Moreover, platelets play an important role in vascular wall remodeling induced by chronic inflammation by controlling vascular cell differentiation and proliferation. In this review, we discuss the role of platelets as cell mediators that link inflammation and thrombosis in atherosclerotic disease and their potential in the development of new therapeutic tools to fight cardiovascular disease.es_ES
dc.description.sponsorshipWork in the author’s laboratories is supported by Centro de Estudios en Alimentos Procesados (CEAP), Conicyt-Regional, Gore Maule, R09I2001, Talca, Chile (Proyecto Basal); The Spanish Ministry of Science and Innovation (MICINN) and the European Regional Development Fund (grant SAF2010-16044); Instituto de Salud Carlos III (ISCIII) (Red de Enfermedades Cardiovasculares [RECAVA], grant RD06/0014/0021). O.M.P. holds a Juan de la Cierva contract (MICINN). The CNIC is supported by the MICINN and the 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.subject.meshAnimals es_ES
dc.subject.meshAtherosclerosis es_ES
dc.subject.meshBlood Platelets es_ES
dc.subject.meshCell Differentiation es_ES
dc.subject.meshEndothelial Cells es_ES
dc.subject.meshHumans es_ES
dc.subject.meshInflammation es_ES
dc.subject.meshStem Cells es_ES
dc.subject.meshThrombosis es_ES
dc.titleRole of platelets as mediators that link inflammation and thrombosis in atherosclerosises_ES
dc.typeArtículoes_ES
dc.rights.licenseAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.identifier.pubmedID22671308es_ES
dc.format.volume24es_ES
dc.format.number4es_ES
dc.format.page255-62es_ES
dc.identifier.doi10.3109/09537104.2012.690113es_ES
dc.contributor.funderCentro de Estudios en Alimentos Procesados (Chile)
dc.contributor.funderMinisterio de Ciencia e Innovación (España)
dc.contributor.funderEuropean Regional Development Fund (ERDF/FEDER)
dc.contributor.funderInstituto de Salud Carlos III - ISCIII
dc.contributor.funderFundación ProCNIC
dc.description.peerreviewedes_ES
dc.identifier.e-issn1369-1635es_ES
dc.relation.publisherversionhttps://doi.org/10.3109/09537104.2012.690113es_ES
dc.identifier.journalPlateletses_ES
dc.repisalud.orgCNICCNIC::Grupos de investigación::Fisiopatología Cardiovascular Molecular y Genéticaes_ES
dc.repisalud.institucionCNICes_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/SAF2010-16044es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/RD06/0014/0021es_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