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. 2021 May 20;12:636175. doi: 10.3389/fendo.2021.636175

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Copyright © 2021 Fang, Liu, Zheng, Guo, Zeng, Huang and Ouyang

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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A proposed model of diabetic kidney disease mediated by bile acids. Bile acids may inhibit endoplasmic reticulum stress, inflammation and fibrosis by activating FXR and TGR5 to improve diabetic kidney disease. BAs, bile acids; FXR, Farnesoid X receptor; TGR5, G protein-coupled receptor 5; ER stress, endoplasmic reticulum stress; NF-κB, nuclear factor kappa-light-chain-enhancer of activated B cells; ICAM-1, intercellular adhesion molecule-1; TGF-β1, transforming growth factor-β1; FN, fibronectin.