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dc.contributor.authorCordero-Barreal, Alfonso
dc.contributor.authorGonzález-Rodríguez, María
dc.contributor.authorRuiz-Fernández, Clara
dc.contributor.authorEldjoudi, Djedjiga Ait
dc.contributor.authorAbdElHafez, Yousof Ramadan Farrag
dc.contributor.authorLago, Francisca
dc.contributor.authorConde, Javier
dc.contributor.authorGómez, Rodolfo
dc.contributor.authorGonzález-Gay Mantecón, Miguel Ángel 
dc.contributor.authorMobasheri, Ali
dc.contributor.authorPino, Jesus
dc.contributor.authorGualillo, Oreste
dc.contributor.otherUniversidad de Cantabriaes_ES
dc.date.accessioned2022-03-30T14:41:02Z
dc.date.available2022-03-30T14:41:02Z
dc.date.issued2021
dc.identifier.issn1661-6596
dc.identifier.issn1422-0067
dc.identifier.urihttp://hdl.handle.net/10902/24454
dc.description.abstractSince its discovery in 1994, leptin has been considered as an adipokine with pleiotropic effects. In this review, we summarize the actual information about the impact of this hormone on cartilage metabolism and pathology. Leptin signalling depends on the interaction with leptin receptor LEPR, being the long isoform of the receptor (LEPRb) the one with more efficient intracellular signalling. Chondrocytes express the long isoform of the leptin receptor and in these cells, leptin signalling, alone or in combination with other molecules, induces the expression of pro-inflammatory molecules and cartilage degenerative enzymes. Leptin has been shown to increase the proliferation and activation of immune cells, increasing the severity of immune degenerative cartilage diseases. Leptin expression in serum and synovial fluid are related to degenerative diseases such as osteoarthritis (OA), rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). Inhibition of leptin signalling showed to have protective effects in these diseases showing the key role of leptin in cartilage degeneration.es_ES
dc.description.sponsorshipAcknowledgments: This work was supported by Xunta de Galicia (Servizo Galego de Saude, SERGAS), through a research-staff contract (ISCIII/SERGAS) to OG and FL, which are Staff Personnel (I3SNS stable Researcher), by Instituto de Salud Carlos III (ISCIII) and by FEDER through a predoctoral research scholar to CR-F (Exp.18/00188), and “Miguel Servet” Researcher contract to RG and JC. MG is a recipient of pre-doctoral contract funded by Xunta de Galicia (IN606A-2020/010). AC is a recipient of a pre-doctoral contract funded by Secretaría de Estado de Universidades, Investigación, Desarrollo e Innovación, Ministerio de Universidades (FPU2018-04165). OG is member of RETICS Programme, [RD16/0012/0014] (RIER: Red de Investigación en Inflamación y Enfermedades Reumáticas) via ISCIII and FEDER. FL is a member of CIBERCV (Centro de Investigación Biomédica en Red de Enfermedades Cardiovasculares). ISCIII and FEDER also support OG and JP [PI17/00409 and PI20/00902]. This work was supported by Research Executive Agency of the European Union in the framework of MSCA-RISE Action of the H2020 Programme [Project number 734899], and Xunta de Galicia, Consellería de Educación, Universidade e Formación Profesional and Consellería de Economía, Emprego e Industria (GAIN) [GPC IN607B2019/10] to OG. A.M. has received funding from the following sources: The European Commission Framework 7 program (EU FP7; HEALTH.2012.2.4.5-2, project number 305815; Novel Diagnostics and Biomarkers for Early Identification of Chronic Inflammatory Joint Diseases). The Innovative Medicines Initiative Joint Undertaking under grant agreement No. 115770, resources of which are composed of financial contribution from the European Union’s Seventh Framework program (FP7/2007-2013) and EFPIA companies’ in-kind contribution. A.M. also wishes to acknowledge funding from the European Commission through a Marie Curie Intra-European Fellowship for Career Development grant (Project number 625746; acronym: CHONDRION; FP7-PEOPLE-2013-IEF). A.M. also wishes to acknowledge financial support from the European Structural and Social Funds (ES Strukt ¯ urin˙ es Paramos) 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-LMTK-712 (grant application code: 09.3.3-LMT-K-712-01-0157, agreement No. DOTSUT-215) and the new funding program: Attracting Foreign Researchers for Research Implementation (2018-2022).es_ES
dc.format.extent16 p.es_ES
dc.language.isoenges_ES
dc.publisherMDPIes_ES
dc.rights© 2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution(CC BY) license.es_ES
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.sourceInt J Mol Sci . 2021 Feb 27;22(5):2411es_ES
dc.subject.otherLeptines_ES
dc.subject.otherArticular cartilagees_ES
dc.subject.otherChondrocytees_ES
dc.subject.otherLEPR (ObR)es_ES
dc.subject.otherOsteoarthritis (OA)es_ES
dc.subject.otherRheumatoid arthritis (RA)es_ES
dc.titleAn update on the role of leptin in the immuno-metabolism of cartilagees_ES
dc.typeinfo:eu-repo/semantics/articlees_ES
dc.relation.publisherVersionhttps://doi.org/10.3390/ ijms22052411es_ES
dc.rights.accessRightsopenAccesses_ES
dc.identifier.DOI10.3390/ijms22052411
dc.type.versionpublishedVersiones_ES


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© 2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution(CC BY) license.Excepto si se señala otra cosa, la licencia del ítem se describe como © 2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution(CC BY) license.