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. 2020 Jun 30;11:967. doi: 10.3389/fphar.2020.00967

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Copyright © 2020 Kawanami and Takashi

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Mechanisms of the renoprotective effects of GLP-1RAs. GLP-1RAs have been shown to activate PKA and increase the production of cyclic adenosine monophosphate (cAMP). As a consequence, nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and NF-κB activity are inhibited, resulting in the attenuation of oxidative stress and inflammation. These favorable effects prevent podocyte loss as well as mesangial and endothelial dysfunction.. GLP-1RAs inactivate NHE3 and promote atrial natriuretic peptide (ANP) secretion, thereby inducing natriuresis. Furthermore, GLP-1RAs inhibit tubular injury and subsequent tubulointerstitial fibrosis.