Show simple item record

dc.contributor.authorAndres, Vicente 
dc.contributor.authorPello, Oscar M 
dc.contributor.authorSilvestre-Roig, Carlos 
dc.date.accessioned2019-05-23T09:51:20Z
dc.date.available2019-05-23T09:51:20Z
dc.date.issued2012-10
dc.identifier.citationCurr Opin Lipidol. 2012; 23(5):429-38es_ES
dc.identifier.issn0957-9672es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/7663
dc.description.abstractPURPOSE OF REVIEW: Atherosclerosis is driven by cardiovascular risk factors that cause the recruitment of circulating immune cells beneath the vascular endothelium. Infiltrated monocytes differentiate into different macrophage subtypes with protective or pathogenic activities in vascular lesions. We discuss current knowledge about the molecular mechanisms that regulate lesional macrophage proliferation and apoptosis, two processes that occur during atherosclerosis development and regulate the number and function of macrophages within the atherosclerotic plaque. RECENT FINDINGS: Lesional macrophages in early phases of atherosclerosis limit disease progression by phagocytizing modified lipoproteins, cellular debris and dead cells that accumulate in the plaque. However, macrophages in advanced lesions contribute to a maladaptive, nonresolving inflammatory response that can lead to life-threatening acute thrombotic diseases (myocardial infarction or stroke). Macrophage-specific manipulation of genes involved in cell proliferation and apoptosis modulates lesional macrophage accumulation and atherosclerosis burden in mouse models, and studies are beginning to elucidate the underlying mechanisms. SUMMARY: Despite recent advances in our understanding of macrophage proliferation and apoptosis in atherosclerotic plaques, it remains unclear whether manipulating these processes will be beneficial or harmful. Advances in these areas may translate into more efficient therapies for the prevention and treatment of atherothrombosis.es_ES
dc.description.sponsorshipWork in the authors’ laboratory is supported by grant SAF2010-16044 from the Ministerio de Economía y Competitividad (MINECO), grant RD06/0014/0021 (RECAVA) from the Instituto de Salud Carlos III, Marie Curie Career Integration Grant PCIG10-GA-2011-303850 from the European Commission, and the Dr. Léon Dumont Prize 2010 from the Belgian Society of Cardiology (to V.A.). C.S. has been supported by Fundación Mario Losantos del Campo and Fundación Ferrer para la Investigación. O.M.P. holds a Juan de la Cierva contract from MINECO. The CNIC is supported by MINECO 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.meshDisease Progression es_ES
dc.subject.meshEndoplasmic Reticulum Stress es_ES
dc.subject.meshGranulocyte-Macrophage Colony-Stimulating Factor es_ES
dc.subject.meshHumans es_ES
dc.subject.meshMacrophage Colony-Stimulating Factor es_ES
dc.subject.meshMacrophages es_ES
dc.subject.meshMice es_ES
dc.subject.meshNecrosis es_ES
dc.subject.meshPhagocytosis es_ES
dc.subject.meshPlaque, Atherosclerotices_ES
dc.subject.meshApoptosis es_ES
dc.subject.meshCell Proliferation es_ES
dc.titleMacrophage proliferation and apoptosis in atherosclerosises_ES
dc.typeArtículoes_ES
dc.rights.licenseAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.identifier.pubmedID22964992es_ES
dc.format.volume23es_ES
dc.format.number5es_ES
dc.format.page429-38es_ES
dc.identifier.doi10.1097/MOL.0b013e328357a379es_ES
dc.contributor.funderMinisterio de Economía y Competitividad (España)es_ES
dc.contributor.funderInstituto de Salud Carlos III - ISCIIIes_ES
dc.contributor.funderEuropean Commissiones_ES
dc.contributor.funderBelgian Society of Cardiologyes_ES
dc.contributor.funderFundación Mario Losantos del Campoes_ES
dc.contributor.funderFundación Ferreres_ES
dc.contributor.funderFundación ProCNICes_ES
dc.description.peerreviewedes_ES
dc.identifier.e-issn1473-6535es_ES
dc.relation.publisherversionhttps://doi.org/10.1097/MOL.0b013e328357a379es_ES
dc.identifier.journalCurrent opinion in lipidologyes_ES
dc.repisalud.orgCNICCNIC::Grupos de investigación::Fisiopatología Cardiovascular Molecular y Genéticaes_ES
dc.repisalud.institucionCNICes_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/EC/FP7/303850/EUes_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


Files in this item

Acceso Abierto
Thumbnail

This item appears in the following Collection(s)

Show simple item record

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