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dc.contributor.authorVarona, Saray
dc.contributor.authorPuertas, Lídia
dc.contributor.authorGalán, María
dc.contributor.authorOrriols, Mar
dc.contributor.authorCañes, Laia
dc.contributor.authorAguiló, Silvia
dc.contributor.authorCamacho, Mercedes
dc.contributor.authorSirvent, Marc
dc.contributor.authorAndres, Vicente 
dc.contributor.authorMartinez-Gonzalez, Jose
dc.contributor.authorRodriguez, Cristina
dc.date.accessioned2021-03-30T09:10:45Z
dc.date.available2021-03-30T09:10:45Z
dc.date.issued2021-03-16
dc.identifier.citationAntioxidants (Basel). 2021; 10(3)es_ES
dc.identifier.issn2076-3921
dc.identifier.urihttp://hdl.handle.net/20.500.12105/12464
dc.description.abstractAbdominal aortic aneurysm (AAA) is a common life-threatening condition characterized by exacerbated inflammation and the generation of reactive oxygen species. Pharmacological treatments to slow AAA progression or to prevent its rupture remain a challenge. Targeting phosphodiesterase 4 (PDE4) has been verified as an effective therapeutic strategy for an array of inflammatory conditions; however, no studies have assessed yet PDE4 in AAA. Here, we used angiotensin II (AngII)-infused apolipoprotein E deficient mice to study the involvement of the PDE4 subfamily in aneurysmal disease. PDE4B but not PDE4D was upregulated in inflammatory cells from both experimental and human AAA. The administration of the PDE4 selective inhibitor rolipram (3 mg/kg/day) to AngII-challenged mice (1000 ng/kg bodyweight/min) protected against AAA formation, limiting the progressive increase in the aortic diameter without affecting the blood pressure. The drug strongly attenuated the rise in vascular oxidative stress (superoxide anion) induced by AngII, and decreased the expression of inflammatory markers, as well as the recruitment of macrophages (MAC3+), lymphocytes (CD3+), and neutrophils (ELANE+) into the vessel wall. Rolipram also normalized the vascular MMP2 expression and MMP activity, preserving the elastin integrity and improving the vascular remodelling. These results point to PDE4B as a new therapeutic target for AAA. View Full-Textes_ES
dc.language.isoenges_ES
dc.publisherMDPIes_ES
dc.relation.isversionofPublisher's versiones_ES
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.titleRolipram Prevents the Formation of Abdominal Aortic Aneurysm (AAA) in Mice: PDE4B as a Target in AAAes_ES
dc.typeArtículoes_ES
dc.rights.licenseAtribución 4.0 Internacional*
dc.format.volume10es_ES
dc.format.number3es_ES
dc.format.page460es_ES
dc.identifier.doi10.3390/antiox10030460es_ES
dc.contributor.funderInstituto de Salud Carlos III - ISCIII
dc.contributor.funderMinisterio de Ciencia e Innovación (España)
dc.contributor.funderAgencia de Gestio d'Ajuts Universitaris i de Recerca
dc.contributor.funderSociedad Española de Arteriosclerosis
dc.contributor.funderSociedad Española de Cardiología
dc.contributor.funderEuropean Regional Development Fund (ERDF/FEDER)
dc.contributor.funderFundación ProCNIC
dc.description.peerreviewedes_ES
dc.relation.publisherversionhttps://doi.org/10.3390/antiox10030460es_ES
dc.identifier.journalAntioxidantses_ES
dc.repisalud.orgCNICCNIC::Grupos de investigación::Fisiopatología Cardiovascular Molecular y Genéticaes_ES
dc.repisalud.institucionCNICes_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/PI18/0919es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/RTI2018-094727-B-100es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/PID2019-108489RB-100es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/2017-SGR-00333es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/SEC/FEC-INV-BAS 20/005es_ES
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses_ES


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