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dc.contributor.authorLavoz, Carolina
dc.contributor.authorRayego Mateos, Sandra
dc.contributor.authorOrejudo, Macarena
dc.contributor.authorOpazo Rios, Lucas
dc.contributor.authorMarchant, Vanessa
dc.contributor.authorMarquez Exposito, Laura
dc.contributor.authorTejera Muñoz, Antonio
dc.contributor.authorNavarro González, Juan F.
dc.contributor.authorDroguett, Alejandra
dc.contributor.authorOrtiz, Alberto
dc.contributor.authorEgido, Jesús
dc.contributor.authorMezzano, Sergio
dc.contributor.authorRodrigues-Diez, Raul
dc.contributor.authorRuiz-Ortega, Marta
dc.description.abstractChronic kidney disease has become a major medical issue in recent years due to its high prevalence worldwide, its association with premature mortality, and its social and economic implications. A number of patients gradually progress to end-stage renal disease (ESRD), requiring then dialysis and kidney transplantation. Currently, approximately 40% of patients with diabetes develop kidney disease, making it the most prevalent cause of ESRD. Thus, more effective therapies for diabetic nephropathy are needed. In preclinical studies of diabetes, anti-inflammatory therapeutic strategies have been used to protect the kidneys. Recent evidence supports that immune cells play an active role in the pathogenesis of diabetic nephropathy. Th17 immune cells and their effector cytokine IL-17A have recently emerged as promising targets in several clinical conditions, including renal diseases. Here, we review current knowledge regarding the involvement of Th17/IL-17A in the genesis of diabetic renal injury, as well as the rationale behind targeting IL-17A as an additional therapy in patients with diabetic nephropathy.ca_ES
dc.description.sponsorshipThis work and data discussed here were supported by grants from the Instituto de Salud Carlos III (ISCIII) and Fondos FEDER European Union (PI17/00119 and Red de Investigacion Renal (REDINREN): RD16/0009, to M.R.-O., PI17/01495, DTS17/00203 and DTS19/00093 to J.E., PI16/02057, PI19/00815 to A.O.); Comunidad de Madrid ("NOVELREN" B2017/BMD-3751 to M.R.-O., B2017/BMD-3686 CIFRA2-CM to A.O.); the Jose Castillejo grant (CAS19/00133 to R.R.R.-D.); the "Juan de la Cierva Formacion" training program of the Ministerio de Economia, Industria y Competitividad (MINECO) supported the salary of S.R.-M. (FJCI-2016-29050); "Convocatoria Dinamizacion Europa Investigacion 2019" MINECO (EIN2019-103294 to M.R.-O. and S.R.-M.); Sociedad Espanola de Nefrologia (S.E.N. to M.R.-O.). Grants Fondecyt 1160465 to S.M. and PAI 82140017 to C.L. of Chile; ERA-PerMed-JTC2018 (KIDNEY ATTACK AC18/00064 and PERSTIGAN AC18/00071) and DTS18/00032 to A.O.; IMPROVE-PD project ("Identification and Management of Patients at Risk-Outcome and Vascular Events in Peritoneal Dialysis") funding from the European Union's Horizon 2020 research and innovation program under the Marie Sklodowska-Curie Grant Agreement No. 812699 to M.R.O.ca_ES
dc.relation.isformatofReproducció del document publicat a
dc.relation.ispartofJournal of clinical medicine, 2020, vol. 9, núm. 1, p.1-17ca_ES
dc.rightscc-by (c) Lavoz et al., 2020ca_ES
dc.subject.otherNefropaties diabètiquesca_ES
dc.subject.otherMalalties cròniques--Diagnòsticca_ES
dc.titleCould IL-17A be a novel therapeutic target in diabetic nephropathy?ca_ES

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cc-by (c) Lavoz et al., 2020
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