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. 2023 Jan 21;11(2):305. doi: 10.3390/biomedicines11020305

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© 2023 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

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Mechanistic model showing a putative role for metformin in inhibiting renal NCC and ENaC activation and reducing blood pressure in the diabetic kidney. An increase in cathepsin B mediated proteolysis of ENaC alpha in distal tubule (DT) and collecting duct (CD) cells, contributes to the development of salt-sensitive hypertension in the diabetic kidney. Hypertension exacerbates the development of diabetic nephropathy. Metformin attenuates Cathepsin B levels in the kidneys and in EVs to alleviate salt-sensitive hypertension in the diabetic kidney. In addition, metformin reduces the density of ENaC at the luminal membrane. MVB refers to multivesicular body.