Lipotoxicity and diabetic nephropathy: Novel mechanistic insights and therapeutic opportunities

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Show simple item record Opazo-Ríos, Lucas Mas, Sebastián Marín-Royo, Gema Mezzano, Sergio Gómez-Guerrero, Carmen Moreno, Juan Antonio Egido, Jesús
dc.contributor.other UAM. Departamento de Medicina es_ES
dc.contributor.other Instituto de Investigación Sanitaria Fundación Jiménez Díaz (ISS-FJD) 2021-02-12T14:15:29Z 2021-02-12T14:15:29Z 2020-04-10
dc.identifier.citation International Journal of Molecular Sciences 21.7 (2020): 2632 en_US
dc.identifier.issn 1661-6596 es_ES
dc.description.abstract Lipotoxicity is characterized by the ectopic accumulation of lipids in organs different from adipose tissue. Lipotoxicity is mainly associated with dysfunctional signaling and insulin resistance response in non-adipose tissue such as myocardium, pancreas, skeletal muscle, liver, and kidney. Serum lipid abnormalities and renal ectopic lipid accumulation have been associated with the development of kidney diseases, in particular diabetic nephropathy. Chronic hyperinsulinemia, often seen in type 2 diabetes, plays a crucial role in blood and liver lipid metabolism abnormalities, thus resulting in increased non-esterified fatty acids (NEFA). Excessive lipid accumulation alters cellular homeostasis and activates lipogenic and glycogenic cell-signaling pathways. Recent evidences indicate that both quantity and quality of lipids are involved in renal damage associated to lipotoxicity by activating inflammation, oxidative stress, mitochondrial dysfunction, and cell-death. The pathological effects of lipotoxicity have been observed in renal cells, thus promoting podocyte injury, tubular damage, mesangial proliferation, endothelial activation, and formation of macrophage-derived foam cells. Therefore, this review examines the recent preclinical and clinical research about the potentially harmful effects of lipids in the kidney, metabolic markers associated with these mechanisms, major signaling pathways affected, the causes of excessive lipid accumulation, and the types of lipids involved, as well as offers a comprehensive update of therapeutic strategies targeting lipotoxicity. en_US
dc.description.sponsorship The authors’ work has been supported by FEDER-ISCIII Funds (PI17/00130, PI17/01495, and SAF2015-63696-R), Spanish Ministry of Economy and Competitiveness (RTI2018-098788-B-100, DTS17/00203, DTS19/00093, and RYC-2017-22369), Fondecyt Project (No. 1160465), Spanish Society of Cardiology (SEC), Spanish Society of Nephrology (SEN), and Spanish Society of Atherosclerosis (SEA). en_US
dc.format.extent 30 pag. es_ES
dc.format.mimetype application/pdf en
dc.language.iso eng en_US
dc.publisher MDPI, Basel, SMwitzerland en_US
dc.relation.ispartof International Journal of Molecular Sciences en_US
dc.rights © 2020 The Authors en_US
dc.subject.other Chronic kidney disease en_US
dc.subject.other Diabetic nephropathy en_US
dc.subject.other Fatty kidney en_US
dc.subject.other Lipotoxicity en_US
dc.subject.other Obesity en_US
dc.subject.other Type 2 diabetes en_US
dc.title Lipotoxicity and diabetic nephropathy: Novel mechanistic insights and therapeutic opportunities en_US
dc.type article en
dc.subject.eciencia Medicina es_ES
dc.relation.publisherversion es_ES
dc.identifier.doi 10.3390/ijms21072632 es_ES
dc.identifier.publicationfirstpage 2632-1 es_ES
dc.identifier.publicationissue 7 es_ES
dc.identifier.publicationlastpage 2632-30 es_ES
dc.relation.projectID Gobierno de España. PI17/00130 es_ES
dc.relation.projectID Gobierno de España. PI17/01495 es_ES
dc.relation.projectID Gobierno de España. SAF2015-63696-R es_ES
dc.relation.projectID Gobierno de España. RTI2018-098788-B-100 es_ES
dc.relation.projectID Gobierno de España. DTS17/00203 es_ES
dc.relation.projectID Gobierno de España. DTS19/00093 es_ES
dc.relation.projectID Gobierno de España. RYC-2017-22369 es_ES
dc.type.version info:eu-repo/semantics/publishedVersion en Reconocimiento es_ES
dc.rights.accessRights openAccess en
dc.authorUAM Gómez Guerrero, Carmen (261179)
dc.authorUAM Egido De Los Ríos, Jesús (259718)

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