Please use this identifier to cite or link to this item: https://accedacris.ulpgc.es/handle/10553/136829
DC FieldValueLanguage
dc.contributor.authorNogueira-Recalde, Uxia-
dc.contributor.authorLambertucci, Flavia-
dc.contributor.authorMontegut, Lea-
dc.contributor.authorMotino, Omar-
dc.contributor.authorChen, Hui-
dc.contributor.authorLachkar, Sylvie-
dc.contributor.authorAnagnostopoulos, Gerasimos-
dc.contributor.authorStoll, Gautier-
dc.contributor.authorLi, Sijing-
dc.contributor.authorCarbonier, Vincent-
dc.contributor.authorSaavedra Díaz, Ester Gloria-
dc.contributor.authorBlanco, Francisco J.-
dc.contributor.authorvan Tetering, Geert-
dc.contributor.authorde Boer, Mark-
dc.contributor.authorMaiuri, Maria Chiara-
dc.contributor.authorCarames, Beatriz-
dc.contributor.authorMartins, Isabelle-
dc.contributor.authorKroemer, Guido-
dc.date.accessioned2025-03-31T14:20:50Z-
dc.date.available2025-03-31T14:20:50Z-
dc.date.issued2025-
dc.identifier.issn1350-9047-
dc.identifier.otherWoS-
dc.identifier.urihttps://accedacris.ulpgc.es/handle/10553/136829-
dc.description.abstractThe plasma concentrations of acyl CoA binding protein (ACBP) encoded by the gene diazepam binding inhibitor (DBI) are increased in patients with severe osteoarthritis (OA). Here, we show that knee OA induces a surge in plasma ACBP/DBI in mice subjected to surgical destabilization of one hind limb. Knockout of the Dbi gene or intraperitoneal (i.p.) injection of a monoclonal antibody (mAb) neutralizing ACBP/DBI attenuates OA progression in this model, supporting a pathogenic role for ACBP/DBI in OA. Furthermore, anti-ACBP/DBI mAb was also effective against OA after its intraarticular (i.a.) injection, as monitored by sonography, revealing the capacity of ACBP/DBI to locally reduce knee inflammation over time. In addition, i.a. anti-ACBP/DBI mAb improved functional outcomes, as indicated by the reduced weight imbalance caused by OA. At the anatomopathological level, i.a. anti-ACBP/DBI mAb mitigated histological signs of joint destruction and synovial inflammation. Of note, i.a. anti-ACBP/DBI mAb blunted the OA-induced surge of plasma ACBP/DBI, as well as that of other inflammatory factors including interleukin-1 alpha, interleukin-33, and tumor necrosis factor. These findings are potentially translatable to OA patients because joints from OA patients express both ACBP/DBI and its receptor GABAAR gamma 2. Moreover, a novel mAb against ACBP/DBI recognizing an epitope conserved between human and mouse ACBP/DBI demonstrated similar efficacy in mitigating OA as an anti-mouse ACBP/DBI-only mAb. In conclusion, ACBP/DBI might constitute a promising therapeutic target for the treatment of OA.-
dc.languageeng-
dc.relation.ispartofCell Death and Differentiation-
dc.sourceCell Death And Differentiation[ISSN 1350-9047], (Marzo 2025)-
dc.subject32 Ciencias médicas-
dc.subject320714 Osteopatología-
dc.subject.otherCartilage Histopathology-
dc.subject.otherHip Osteoarthritis-
dc.subject.otherAutophagy-
dc.subject.otherKnee-
dc.subject.otherExpression-
dc.subject.otherArthritis-
dc.subject.otherGenetics-
dc.subject.otherBurden-
dc.subject.otherModel-
dc.titleNeutralization of acyl CoA binding protein (ACBP) for the experimental treatment of osteoarthritis-
dc.typeinfo:eu-repo/semantics/Article-
dc.typeArticle-
dc.identifier.doi10.1038/s41418-025-01474-y-
dc.identifier.scopus105000038954-
dc.identifier.isi001445953300001-
dc.contributor.orcidNO DATA-
dc.contributor.orcidNO DATA-
dc.contributor.orcid0000-0003-4778-4757-
dc.contributor.orcid0000-0002-3858-0966-
dc.contributor.orcid0000-0002-1260-8617-
dc.contributor.orcidNO DATA-
dc.contributor.orcid0000-0002-2042-8675-
dc.contributor.orcid0000-0002-0862-4139-
dc.contributor.orcidNO DATA-
dc.contributor.orcidNO DATA-
dc.contributor.orcidNO DATA-
dc.contributor.orcid0000-0001-9821-7635-
dc.contributor.orcidNO DATA-
dc.contributor.orcidNO DATA-
dc.contributor.orcidNO DATA-
dc.contributor.orcidNO DATA-
dc.contributor.orcid0000-0003-0885-613X-
dc.contributor.orcid0000-0002-9334-4405-
dc.contributor.authorscopusid57190284281-
dc.contributor.authorscopusid57192204244-
dc.contributor.authorscopusid57216393606-
dc.contributor.authorscopusid55321968400-
dc.contributor.authorscopusid57214092108-
dc.contributor.authorscopusid57202998114-
dc.contributor.authorscopusid57210949777-
dc.contributor.authorscopusid8754407600-
dc.contributor.authorscopusid57225968775-
dc.contributor.authorscopusid59693878200-
dc.contributor.authorscopusid59693325600-
dc.contributor.authorscopusid7102243071-
dc.contributor.authorscopusid14827606000-
dc.contributor.authorscopusid58500363500-
dc.contributor.authorscopusid6506604201-
dc.contributor.authorscopusid8594051200-
dc.contributor.authorscopusid22944783100-
dc.contributor.authorscopusid35380287000-
dc.identifier.eissn1476-5403-
dc.investigacionCiencias de la Salud-
dc.type2Artículo-
dc.contributor.daisngidNo ID-
dc.contributor.daisngidNo ID-
dc.contributor.daisngidNo ID-
dc.contributor.daisngidNo ID-
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dc.contributor.daisngidNo ID-
dc.contributor.daisngidNo ID-
dc.contributor.daisngidNo ID-
dc.contributor.daisngidNo ID-
dc.contributor.daisngidNo ID-
dc.contributor.daisngidNo ID-
dc.contributor.daisngidNo ID-
dc.contributor.daisngidNo ID-
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dc.contributor.daisngidNo ID-
dc.contributor.daisngidNo ID-
dc.description.numberofpages15-
dc.utils.revision-
dc.contributor.wosstandardWOS:Nogueira-Recalde, U-
dc.contributor.wosstandardWOS:Lambertucci, F-
dc.contributor.wosstandardWOS:Montégut, L-
dc.contributor.wosstandardWOS:Motiño, O-
dc.contributor.wosstandardWOS:Chen, H-
dc.contributor.wosstandardWOS:Lachkar, S-
dc.contributor.wosstandardWOS:Anagnostopoulos, G-
dc.contributor.wosstandardWOS:Stoll, G-
dc.contributor.wosstandardWOS:Li, SJ-
dc.contributor.wosstandardWOS:Carbonier, V-
dc.contributor.wosstandardWOS:Díaz, ES-
dc.contributor.wosstandardWOS:Blanco, FJ-
dc.contributor.wosstandardWOS:van Tetering, G-
dc.contributor.wosstandardWOS:de Boer, M-
dc.contributor.wosstandardWOS:Maiuri, MC-
dc.contributor.wosstandardWOS:Caramés, B-
dc.contributor.wosstandardWOS:Martins, I-
dc.contributor.wosstandardWOS:Kroemer, G-
dc.date.coverdateMarzo 2025-
dc.identifier.ulpgc-
dc.contributor.buulpgcBU-MED-
dc.description.sjr4,102-
dc.description.jcr13,7-
dc.description.sjrqQ1-
dc.description.jcrqQ1-
dc.description.scieSCIE-
dc.description.miaricds10,9-
item.grantfulltextopen-
item.fulltextCon texto completo-
crisitem.author.deptGIR IUIBS: Bioquímica-
crisitem.author.deptIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.deptDepartamento de Bioquímica y Biología Molecular, Fisiología, Genética e Inmunología-
crisitem.author.orcid0000-0002-1717-386X-
crisitem.author.parentorgIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.fullNameSaavedra Díaz, Ester Gloria-
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