Mostrar el registro sencillo

dc.contributor.authorFrancisco, Vera
dc.contributor.authorRuiz-Fernández, Clara
dc.contributor.authorPino, Jesús
dc.contributor.authorMera, Antonio
dc.contributor.authorGonzález-Gay Mantecón, Miguel Ángel 
dc.contributor.authorGómez, Rodolfo
dc.contributor.authorLago, Francisca
dc.contributor.authorMobasheri, Ali
dc.contributor.authorGualillo, Oreste
dc.contributor.otherUniversidad de Cantabriaes_ES
dc.date.accessioned2019-06-21T14:36:01Z
dc.date.available2020-07-01T02:45:12Z
dc.date.issued2019-07
dc.identifier.issn0006-2952
dc.identifier.issn1873-2968
dc.identifier.urihttp://hdl.handle.net/10902/16371
dc.description.abstractMetabolic syndrome (MetS) represents a cluster of metabolic and cardiovascular complications, including obesity and visceral adiposity, insulin resistance, dyslipidemia, hyperglycemia and hypertension, which directly increase the risk of cardiovascular diseases (CVD) and diabetes mellitus type 2 (DM2). Patients with arthritic diseases, such as rheumatoid arthritis and osteoarthritis, have a higher incidence of CVD. Although recent advances in the treatment of arthritic diseases, the incidence of CVD remains elevated, and MetS has been identified as a possible link between CVD and arthritic diseases. Chronic low-grade inflammation associated with obesity has been established as a significant contributing factor to the increased prevalence of MetS. Adipokines, which play important physiological roles in metabolic activities contributing to the pathogenesis of MetS, are also involved in the regulation of autoimmune and/or inflammatory processes associated with arthritic diseases. Therefore, MetS and dysregulated secretion of pro-inflammatory adipokines have been recognized as a molecular link between CVD and arthritis diseases. In the present paper, we review recent evidence supporting the role played by adipokines, in particular leptin, adiponectin, and lipocalin-2, in the modulation of the immune system, MetS and arthritic diseases. The underlying cellular and molecular mechanisms are discussed, as well as potential new therapeutic strategies.es_ES
dc.description.sponsorshipAcknowledgments: OG and FL are Staff Personnel of Xunta de Galicia (Servizo Galego de Saude, SERGAS) through a research-staff stabilization contract (ISCIII/SERGAS). VF is a “Sara Borrell” Researcher funded by ISCIII and FEDER (CD16/00111). RG is a “Miguel Servet” Researcher funded by Instituto de Salud Carlos III (ISCIII) and FEDER. CRF is a pre-doctoral research scholar funded by ISCIII and FEDER (Exp.18/00188). OG, MAGG, and RG are members of RETICS Programme, RD16/0012/0014 (RIER: Red de Investigación en Inflamación y Enfermedades Reumáticas) via Instituto de Salud Carlos III (ISCIII) and FEDER. FL is a member of CIBERCV (Centro de Investigación Biomédica en Red de Enfermedades Cardiovasculares). The work of OG and JP (PI17/00409), RG (PI16/01870 and CP15/00007) and FL (PI15/00681 PI18/00821 and CB16/11/00226) were funded by Instituto de Salud Carlos III and FEDER. OG is a beneficiary of a project funded by Research Executive Agency of the European Union in the framework of MSCA-RISE Action of the H2020 Programme (Project number 734899). RG is beneficiary of a project funded by Mutua Madrileña 2018. AM wishes to acknowledge financial support from the European Structural and Social Funds through the Research Council of Lithuania (Lietuvos Mokslo Taryba) according to the activity ‘Improvement of researchers’ qualification by implementing world-class R&D projects’ of Measure No. 09.3.3-LMT-K-712 (grant application code: 09.3.3-LMT-K-712-01-0157, agreement No. DOTSUT-215) and the new funding programme: Attracting Foreign Researchers for Research Implementation (2018–2022). The funders had no role in study design, data collection, and analysis, decision to publish, or preparation of the manuscript.es_ES
dc.format.extent11 p.es_ES
dc.language.isoenges_ES
dc.publisherElsevieres_ES
dc.rights© 2019. This manuscript version is made available under the CC-BY-NC-ND 4.0 licensees_ES
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.sourceBiochem Pharmacol. 2019 Jul;165:196-206es_ES
dc.subject.otherAdiponectines_ES
dc.subject.otherInflammationes_ES
dc.subject.otherLeptines_ES
dc.subject.otherLipocalin-2es_ES
dc.subject.otherMetabolic Syndromees_ES
dc.subject.otherObesityes_ES
dc.subject.otherOsteoarthritises_ES
dc.subject.otherRheumatoid Arthritises_ES
dc.titleAdipokines: Linking metabolic syndrome, the immune system, and arthritic diseaseses_ES
dc.typeinfo:eu-repo/semantics/articlees_ES
dc.relation.publisherVersionhttps://doi.org/10.1016/j.bcp.2019.03.030es_ES
dc.rights.accessRightsopenAccesses_ES
dc.identifier.DOI10.1016/j.bcp.2019.03.030
dc.type.versionacceptedVersiones_ES


Ficheros en el ítem

Thumbnail

Este ítem aparece en la(s) siguiente(s) colección(ones)

Mostrar el registro sencillo

© 2019. This manuscript version is made available under the CC-BY-NC-ND 4.0 licenseExcepto si se señala otra cosa, la licencia del ítem se describe como © 2019. This manuscript version is made available under the CC-BY-NC-ND 4.0 license