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. 2023 Apr 13;22:86. doi: 10.1186/s12933-023-01816-5

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© The Author(s) 2023

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 2 — SGLT2i can improve vasodilatory inflammation by decreasing uric acid levels. In proximal renal tubules, SGLT2i acts on SGLT2, decreasing the reabsorption of Na ions and glucose and increasing glucose concentrations in the lumen, which is exchanged with uric acid by GLUT9 isoform 2. This leads to increased uric acid exclusion. In the collecting duct, high levels of glucose inhibit this exchange and reduce the absorption of uric acid, thereby draining it. Lowering the concentration of uric acid in the blood helps reduce inflammation in the blood vessels