| Literature DB >> 33467524 |
Cristina Vázquez-Carballo1, Melania Guerrero-Hue2, Cristina García-Caballero2, Sandra Rayego-Mateos1, Lucas Opazo-Ríos1,3, José Luis Morgado-Pascual2, Carmen Herencia-Bellido1, Mercedes Vallejo-Mudarra2, Isabel Cortegano4, María Luisa Gaspar4, Belén de Andrés4, Jesús Egido1,3, Juan Antonio Moreno2,5,6.
Abstract
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.Entities:
Keywords: acute kidney injury; drugs; inflammation; therapy; toll-like receptors
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Year: 2021 PMID: 33467524 PMCID: PMC7830297 DOI: 10.3390/ijms22020816
Source DB: PubMed Journal: Int J Mol Sci ISSN: 1422-0067 Impact factor: 5.923