English   español  
Please use this identifier to cite or link to this item: http://hdl.handle.net/10261/170723
Share/Impact:
Statistics
logo share SHARE logo core CORE   Add this article to your Mendeley library MendeleyBASE

Visualizar otros formatos: MARC | Dublin Core | RDF | ORE | MODS | METS | DIDL
Exportar a otros formatos:

DC FieldValueLanguage
dc.contributor.authorDelgado-Maroto, V.es_ES
dc.contributor.authorBenitez, Raqueles_ES
dc.contributor.authorForte-Lago, Irenees_ES
dc.contributor.authorMorell, M.es_ES
dc.contributor.authorMaganto-Garcia, Elenaes_ES
dc.contributor.authorSouza-Moreira, L.es_ES
dc.contributor.authorO’Valle, Franciscoes_ES
dc.contributor.authorDurán-Prado, M.es_ES
dc.contributor.authorAndrew H. Lichtmanes_ES
dc.contributor.authorGonzález-Rey, Elenaes_ES
dc.contributor.authorDelgado, M.es_ES
dc.date.accessioned2018-10-08T09:10:50Z-
dc.date.available2018-10-08T09:10:50Z-
dc.date.issued2017-04-13-
dc.identifier.citationScientific Reportses_ES
dc.identifier.issn2045-2322-
dc.identifier.urihttp://hdl.handle.net/10261/170723-
dc.description.abstractAtherosclerosis is a chronic inflammatory cardiovascular disease that is responsible of high mortality worldwide. Evidence indicates that maladaptive autoimmune responses in the arterial wall play critical roles in the process of atherosclerosis. Cortistatin is a neuropeptide expressed in the vascular system and atherosclerotic plaques that regulates vascular calcification and neointimal formation, and inhibits inflammation in different experimental models of autoimmune diseases. Its role in inflammatory cardiovascular disorders is largely unexplored. The aim of this study is to investigate the potential therapeutic effects of cortistatin in two well-established preclinical models of atherosclerosis, and the molecular and cellular mechanisms involved. Systemic treatment with cortistatin reduced the number and size of atherosclerotic plaques in carotid artery, heart, aortic arch and aorta in acute and chronic atherosclerosis induced in apolipoprotein E-deficient mice fed a high-lipid diet. This effect was exerted at multiple levels. Cortistatin reduced Th1/Th17-driven inflammatory responses and increased regulatory T cells in atherosclerotic arteries and lymphoid organs. Moreover, cortistatin reduced the capacity of endothelial cells to bind and recruit immune cells to the plaque and impaired the formation of foam cells by enhancing cholesterol efflux from macrophages. Cortistatin emerges as a new candidate for the treatment of the clinical manifestations of atherosclerosises_ES
dc.description.sponsorshipThis work was supported by Spanish Ministry of Economy and Competitiveness, Excellence Program from Junta de Andalucia and JAE-Predoc fellowshipes_ES
dc.language.isoenges_ES
dc.publisherSpringeres_ES
dc.relation.isversionofPublisher's versiones_ES
dc.rightsopenAccesses_ES
dc.titleCortistatin reduces atherosclerosis in hyperlipidemic ApoE-deficient mice and the formation of foam cellses_ES
dc.typeartículoes_ES
dc.identifier.doi10.1038/srep46444-
dc.description.peerreviewedPeer reviewedes_ES
dc.relation.publisherversionhttps://www.nature.com/articles/srep46444#abstractes_ES
dc.rights.licensehttp://creativecommons.org/licenses/by/4.0/es_ES
dc.relation.csices_ES
oprm.item.hasRevisionno ko 0 false*
dc.contributor.orcidGonzález-Rey, Elena [0000-0003-3917-9020]es_ES
dc.contributor.orcidDelgado, M. [0000-0003-1893-5982]es_ES
dc.contributor.orcidDelgado-Maroto, V. [0000-0002-2503-5707]es_ES
dc.contributor.orcidSouza-Moreira, L. [0000-0002-1871-4402]es_ES
dc.contributor.orcidO'Valle, Francisco [0000-0001-9207-2287]es_ES
Appears in Collections:(IPBLN) Artículos
Files in This Item:
File Description SizeFormat 
Cortistatin_srep46444.pdfArticle1,86 MBAdobe PDFThumbnail
View/Open
Supplementary_srep46444-s1.pdfSupplementary information1,43 MBAdobe PDFThumbnail
View/Open
Show simple item record
 

Related articles:


WARNING: Items in Digital.CSIC are protected by copyright, with all rights reserved, unless otherwise indicated.