RT Journal Article
T1 Toll-Like Receptors in Acute Kidney Injury
A1 Vázquez Carballo, Cristina
A1 Guerrero Hue, Melania
A1 García Caballero, Cristina G.
A1 Rayego Mateos, Sandra
A1 Opazo Ríos, Lucas
A1 Morgado Pascual, José Luis
A1 Herencia Bellido, Carmen
A1 Vallejo Mudarra, Mercedes
A1 Cortegano Jimeno, María Isabel
A1 Gaspar, María Luisa
A1 De Andrés, Belén
A1 Egido, Jesús
A1 Moreno González De Eiris, Elena
AB Acute kidney injury (AKI) is an important health problem, affecting 13.3 million individuals/year. It is associated with increased mortality, mainly in low- and middle-income countries, where renal replacement therapy is limited. Moreover, survivors show adverse long-term outcomes, including increased risk of developing recurrent AKI bouts, cardiovascular events, and chronic kidney disease. However, there are no specific treatments to decrease the adverse consequences of AKI. Epidemiological and preclinical studies show the pathological role of inflammation in AKI, not only at the acute phase but also in the progression to chronic kidney disease. Toll-like receptors (TLRs) are key regulators of the inflammatory response and have been associated to many cellular processes activated during AKI. For that reason, a number of anti-inflammatory agents targeting TLRs have been analyzed in preclinical studies to decrease renal damage during AKI. In this review, we updated recent knowledge about the role of TLRs, mainly TLR4, in the initiation and development of AKI as well as novel compounds targeting these molecules to diminish kidney injury associated to this pathological condition.
PB MDPI
SN 1422-0067
YR 2021
FD 2021-01-11
LK https://hdl.handle.net/20.500.14352/7350
UL https://hdl.handle.net/20.500.14352/7350
LA eng
NO Vázquez Carballo, C., Guerrero Hue, M., García Caballero, C. G. et al. «Toll-Like Receptors in Acute Kidney Injury». International Journal of Molecular Sciences, vol. 22, n.o 2, enero de 2021, p. 816. DOI.org (Crossref), https://doi.org/10.3390/ijms22020816.
NO The authors work has been supported by grants from Instituto de Salud Carlos III (ISCIII, FIS-FEDER PI17/00130, PI17/01495, PI20/00375, PI20/00487), Spanish Biomedical Research Centre in Diabetes and Associated Metabolic Disorders (CIBERDEM) and Cardiovascular (CIBERCV), Spanish Ministry of Science and Innovation (RTI2018-099114-B-100, RTI2018-098788-B-100, 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.
NO Ministerio de Ciencia, Innovación y Universidades (España)
NO Instituto de Salud Carlos III
NO Centro Español de Investigación Biomédica en Diabetes y Trastornos Metabólicos Asociados
NO Centro Español de Investigación Biomédica en Red. Enfermedades Cardiovasculares
NO Sociedades Españolas de Cardiología
NO Sociedades Españolas de Nefrología
NO Sociedades Españolas de Aterosclerosis
DS Docta Complutense
RD 8 abr 2025