Publication:
Toll-Like Receptors in Acute Kidney Injury.

dc.contributor.authorVázquez-Carballo, Cristina
dc.contributor.authorGuerrero-Hue, Melania
dc.contributor.authorGarcía-Caballero, Cristina
dc.contributor.authorRayego-Mateos, Sandra
dc.contributor.authorOpazo-Ríos, Lucas
dc.contributor.authorMorgado-Pascual, José Luis
dc.contributor.authorHerencia-Bellido, Carmen
dc.contributor.authorVallejo-Mudarra, Mercedes
dc.contributor.authorCortegano, Isabel
dc.contributor.authorGaspar, Maria Luisa
dc.contributor.authorAndres, Belen de
dc.contributor.authorEgido, Jesús
dc.contributor.authorMoreno, Juan Antonio
dc.contributor.funderInstituto de Salud Carlos III
dc.contributor.funderMinisterio de Ciencia e Innovación (España)
dc.contributor.funderSociedad Española de Cardiología
dc.contributor.funderSociedad Española de Nefrología
dc.contributor.funderSociedad Española de Arteriosclerosis
dc.contributor.funderUniversity of Córdoba (España)
dc.date.accessioned2021-04-16T16:49:50Z
dc.date.available2021-04-16T16:49:50Z
dc.date.issued2021-01-15
dc.description.abstractAcute 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.es_ES
dc.description.peerreviewedes_ES
dc.description.sponsorshipThe 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 other relevant affiliations or financial involvement exist with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.es_ES
dc.format.number2es_ES
dc.format.volume22es_ES
dc.identifier.citationInt J Mol Sci . 2021 Jan 15;22(2):816.es_ES
dc.identifier.doi10.3390/ijms22020816es_ES
dc.identifier.e-issn1422-0067es_ES
dc.identifier.journalInternational journal of molecular scienceses_ES
dc.identifier.pubmedID33467524es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/12680
dc.language.isoenges_ES
dc.publisherMultidisciplinary Digital Publishing Institute (MDPI)
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/PI17/00130es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/PI17/01495es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/PI20/00375es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/PI20/00487es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/RTI2018-099114-B-100es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/RTI2018-098788-B-100es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/DTS19/00093es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/RYC-2017-22369es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/FI18/00310es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/CD19/00021es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/CP16/00017es_ES
dc.relation.publisherversionhttps://doi.org/10.3390/ijms22020816es_ES
dc.repisalud.centroISCIII::Centro Nacional de Microbiologíaes_ES
dc.repisalud.institucionISCIIIes_ES
dc.rights.accessRightsopen accesses_ES
dc.rights.licenseAtribución 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subjectAcute kidney injuryes_ES
dc.subjectDrugses_ES
dc.subjectInflammationes_ES
dc.subjectTherapyes_ES
dc.subjectToll-like receptorses_ES
dc.titleToll-Like Receptors in Acute Kidney Injury.es_ES
dc.typejournal articlees_ES
dc.type.hasVersionVoRes_ES
dspace.entity.typePublication
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