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dc.contributor.authorAndres, Vicente 
dc.contributor.authorPello, Oscar M 
dc.contributor.authorSilvestre-Roig, Carlos
dc.identifier.citationCurr Opin Lipidol. 2012; 23(5):429-38es_ES
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.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.typejournal articlees_ES
dc.rights.licenseAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.contributor.funderMinisterio de Economía y Competitividad (España) 
dc.contributor.funderInstituto de Salud Carlos III 
dc.contributor.funderUnión Europea. Comisión Europea 
dc.contributor.funderBelgian Society of Cardiology 
dc.contributor.funderFundación Mario Losantos del Campo 
dc.contributor.funderFundación Ferrer Investigación 
dc.contributor.funderFundación ProCNIC 
dc.identifier.journalCurrent opinion in lipidologyes_ES
dc.repisalud.orgCNICCNIC::Grupos de investigación::Fisiopatología Cardiovascular Molecular y Genéticaes_ES
dc.rights.accessRightsopen accesses_ES

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