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dc.contributor.authorRayego-Mateos, Sandra
dc.contributor.authorMorgado-Pascual, José Luis
dc.contributor.authorOpazo-Ríos, Lucas
dc.contributor.authorGuerrero-Hue, Melania
dc.contributor.authorGarcía-Caballero, Cristina
dc.contributor.authorVázquez-Carballo, Cristina
dc.contributor.authorMas, Sebastián
dc.contributor.authorSanz, Ana Belén
dc.contributor.authorHerencia, Carmen
dc.contributor.authorMezzano, Sergio
dc.contributor.authorGómez-Guerrero, Carmen
dc.contributor.authorMoreno, Juan Antonio
dc.contributor.authorEgido, Jesús
dc.date.accessioned2020-05-27T18:02:29Z
dc.date.available2020-05-27T18:02:29Z
dc.date.issued2020
dc.identifier.urihttp://hdl.handle.net/10396/20032
dc.description.abstractDiabetic nephropathy (DN) is associated with an increased morbidity and mortality, resulting in elevated cost for public health systems. DN is the main cause of chronic kidney disease (CKD) and its incidence increases the number of patients that develop the end-stage renal disease (ESRD). There are growing epidemiological and preclinical evidence about the close relationship between inflammatory response and the occurrence and progression of DN. Several anti-inflammatory strategies targeting specific inflammatory mediators (cell adhesion molecules, chemokines and cytokines) and intracellular signaling pathways have shown beneficial effects in experimental models of DN, decreasing proteinuria and renal lesions. A number of inflammatory molecules have been shown useful to identify diabetic patients at high risk of developing renal complications. In this review, we focus on the key role of inflammation in the genesis and progression of DN, with a special interest in effector molecules and activated intracellular pathways leading to renal damage, as well as a comprehensive update of new therapeutic strategies targeting inflammation to prevent and/or retard renal injury.es_ES
dc.format.mimetypeapplication/pdfes_ES
dc.language.isoenges_ES
dc.publisherMDPIes_ES
dc.rightshttps://creativecommons.org/licenses/by-nc-nd/4.0/es_ES
dc.sourceInternational Journal of Molecular Sciences 21(11), 3798 (2020)es_ES
dc.subjectInflammationes_ES
dc.subjectType 2 diabeteses_ES
dc.subjectDiabetic nephropathyes_ES
dc.subjectChronic kidney diseasees_ES
dc.subjectInflammationes_ES
dc.subjectDrugses_ES
dc.subjectTherapyes_ES
dc.titlePathogenic Pathways and Therapeutic Approaches Targeting Inflammation in Diabetic Nephropathyes_ES
dc.typeinfo:eu-repo/semantics/articlees_ES
dc.relation.publisherversionhttp://dx.doi.org/10.3390/ijms21113798es_ES
dc.relation.projectIDInstituto de Salud Carlos III. PI17/00130es_ES
dc.relation.projectIDInstituto de Salud Carlos III. PI17/01495es_ES
dc.relation.projectIDInstituto de Salud Carlos III. PI19/00588es_ES
dc.relation.projectIDGobierno de España. RTI2018-098788-B-100es_ES
dc.relation.projectIDGobierno de España. DTS17/00203es_ES
dc.relation.projectIDGobierno de España. DTS19/00093es_ES
dc.relation.projectIDGobierno de España. RYC-2017-22369es_ES
dc.relation.projectIDInstituto de Salud Carlos III. FI18/00310es_ES
dc.relation.projectIDInstituto de Salud Carlos III. CD19/00021es_ES
dc.relation.projectIDInstituto de Salud Carlos III. CP16/00017es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/EC/H2020/779282 (PERSTIGAN)es_ES
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses_ES


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