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Pathogenic pathways and therapeutic approaches targeting inflammation in diabetic nephropathy

Author
Rayego-Mateos, Sandra; Morgado-Pascual, José Luis; Opazo-Ríos, Lucas; Guerrero-Hue, Melania; García-Caballero, Cristina; Vázquez-Carballo, Cristina; Mas, Sebastián; Sanz, Ana Belén; Herencia, Carmen; Mezzano, Sergio; Gómez-Guerrero, Carmen; Moreno, Juan Antonio; Egido, Jesús
Entity
UAM. Departamento de Medicina; Instituto de Investigación Sanitaria Fundación Jiménez Díaz (ISS-FJD)
Publisher
MDPI, Basel, SMwitzerland
Date
2020-06-01
Citation
10.3390/ijms21113798
International Journal of Molecular Sciences 21.11 (2020): 3798
 
 
 
ISSN
1661-6596
DOI
10.3390/ijms21113798
Funded by
The authors work has been supported by grants from Instituto de Salud Carlos III (ISCIII, FIS-FEDER PI17/00130, PI17/01495, PI19/00588, ERA-PerMed-JTC2018-PERSTIGAN AC18/00071), Spanish Biomedical Research Centre in Diabetes and Associated Metabolic Disorders (CIBERDEM) and Cardiovascular (CIBERCV), Fondecyt Project (No. 1160465), Spanish Ministry of Science and Innovation (RTI2018-098788-B-100, DTS17/00203, DTS19/00093, RYC-2017-22369), and Spanish Societies of Cardiology (SEC), Nephrology (SEN) and Atherosclerosis (SEA). The “PFIS” and “Sara Borrell” training program of the ISCIII supported the salary of MGH (FI18/00310), SR-M (CD19/00021) and CH-B (CP16/00017). Córdoba University supported the salary of C.G.C.
Project
Gobierno de España. PI17/00130; Gobierno de España. PI17/01495; Gobierno de España. PI19/00588; info:eu-repo/grantAgreement/EC/H2020/779282/EU//ERA-PerMed; Gobierno de España. RTI2018-098788-B-100; Gobierno de España. DTS17/00203; Gobierno de España. DTS19/00093; Gobierno de España. RYC-2017-22369
Editor's Version
http://doi.org/10.3390/ijms21113798
Subjects
And therapy; Chronic kidney disease; Diabetic nephropathy; Drugs; Inflammation; Type 2 diabetes; Medicina
URI
http://hdl.handle.net/10486/694177
Rights
© 2020 The Authors

Licencia Creative Commons
Esta obra está bajo una Licencia Creative Commons Atribución 4.0 Internacional.

Abstract

Diabetic 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 antiinflammatory 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.
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Google™ Scholar:Rayego-Mateos, Sandra - Morgado-Pascual, José Luis - Opazo-Ríos, Lucas - Guerrero-Hue, Melania - García-Caballero, Cristina - Vázquez-Carballo, Cristina - Mas, Sebastián - Sanz, Ana Belén - Herencia, Carmen - Mezzano, Sergio - Gómez-Guerrero, Carmen - Moreno, Juan Antonio - Egido, Jesús

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  • Producción científica en acceso abierto de la UAM [14728]

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