Mañana, JUEVES, 24 DE ABRIL, el sistema se apagará debido a tareas habituales de mantenimiento a partir de las 9 de la mañana. Lamentamos las molestias.
Interleukin-17A blockade reduces albuminuria and kidney injury in an accelerated model of diabetic nephropathy
dc.contributor.author | Lavoz, Carolina | |
dc.contributor.author | Sánchez Matus, Yenniffer | |
dc.contributor.author | Orejudo, Macarena | |
dc.contributor.author | Carpio, J. Daniel | |
dc.contributor.author | Droguett, Alejandra | |
dc.contributor.author | Egido, Jesús | |
dc.contributor.author | Mezzano, Sergio | |
dc.contributor.author | Ruiz Ortega, Marta | |
dc.contributor.author | Instituto de Investigación Sanitaria Fundación Jiménez Díaz (ISS-FJD) | |
dc.contributor.other | UAM. Departamento de Medicina | es_ES |
dc.date.accessioned | 2019-10-08T13:02:44Z | |
dc.date.available | 2019-10-08T13:02:44Z | |
dc.date.issued | 2019-03-08 | |
dc.identifier.citation | Kidney International 95 (2019): 1418–1432 | en_US |
dc.identifier.issn | 0085-2538 (print) | es_ES |
dc.identifier.issn | 1523-1755 (online) | es_ES |
dc.identifier.uri | http://hdl.handle.net/10486/688802 | |
dc.description.abstract | Diabetic nephropathy (DN) is one of the most common complications of diabetes, and currently the first end-stage renal disease worldwide. New strategies to treat DN using agents that target inflammatory pathways have attracted special interest. Recent pieces of evidences suggest a promising effect of IL-17A, the Th17 effector cytokine. Among experimental DN models, mouse strain BTBR ob/ob (leptin deficiency mutation) develops histological features similar to human DN, which means an opportunity to study mechanisms and novel therapies aimed at DN regression. We found that BTBR ob/ob mice presented renal activation of the factors controlling Th17 differentiation. The presence of IL-17A-expressing cells, mainly CD4D and gd lymphocytes, was associated with upregulation of proinflammatory factors, macrophage infiltration and the beginning of renal damage. To study IL-17A involvement in experimental DN pathogenesis, treatment with an IL-17A neutralizing antibody was carried out starting when the renal damage had already appeared. IL-17A blockade ameliorated renal dysfunction and disease progression in BTBR ob/ob mice. These beneficial effects correlated to podocyte number restoration and inhibition of NF-kB/ proinflammatory factors linked to a decrease in renal inflammatory-cell infiltration. These data demonstrate that IL-17A takes part in diabetes-mediated renal damage and could be a promising therapeutic target to improve DN. | en_US |
dc.description.sponsorship | This work was supported by grants PAI 82140017 to CL; Fondecyt 1160465 to SM; Division of Nephrology, Universidad Austral de Chile, the Instituto de Salud Carlos III and FEDER European Union funds (PI14/00041, PI17/00119 to MR-O, and PI14/00386 and PI17/01495 to JE); Red de Investigación Renal (REDinREN; RD16/009) and Comunidad de Madrid (B2017/BMD-3751 NOVELREN-CM) to MR-O, and Sociedad Española de Nefrología | en_US |
dc.format.extent | 15 pag. | es_ES |
dc.format.mimetype | application/pdf | en |
dc.language.iso | eng | en |
dc.publisher | Elsevier Inc. | en_US |
dc.relation.ispartof | Kidney International | en_US |
dc.rights | © 2019 International Society of Nephrology | en_US |
dc.subject.other | BTBR ob/ob | en_US |
dc.subject.other | Diabetic nephropathy | en_US |
dc.subject.other | IL-17A | en_US |
dc.subject.other | Inflammation | en_US |
dc.title | Interleukin-17A blockade reduces albuminuria and kidney injury in an accelerated model of diabetic nephropathy | en_US |
dc.type | article | en |
dc.subject.eciencia | Medicina | es_ES |
dc.relation.publisherversion | https://doi.org/10.1016/ j.kint.2018.12.031 | es_ES |
dc.identifier.doi | 10.1016/ j.kint.2018.12.031 | es_ES |
dc.identifier.publicationfirstpage | 1418 | es_ES |
dc.identifier.publicationissue | 95 | es_ES |
dc.identifier.publicationlastpage | 1432 | es_ES |
dc.relation.projectID | Gobierno de España. PI14/00041 | es_ES |
dc.relation.projectID | Gobierno de España. PI17/00119 | es_ES |
dc.relation.projectID | Gobierno de España. PI14/00386 | es_ES |
dc.relation.projectID | Gobierno de España. PI17/01495 | es_ES |
dc.relation.projectID | Comunidad de Madrid. B2017/BMD-3751/NOVELREN | es_ES |
dc.type.version | info:eu-repo/semantics/publishedVersion | en |
dc.rights.cc | Reconocimiento – NoComercial – SinObraDerivada | es_ES |
dc.rights.accessRights | openAccess | en |
dc.authorUAM | Ruiz Ortega, Marta (260902) | |
dc.authorUAM | Egido De Los Ríos, Jesús (259718) | |
dc.facultadUAM | Facultad de Medicina | |
dc.institutoUAM | Instituto de Investigación Sanitaria Fundación Jiménez Díaz (ISS-FJD) |