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. 2021 Mar 30;12:630617. doi: 10.3389/fphar.2021.630617

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Copyright © 2021 Wang and He.

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 underlying renal cell damage associated with dysregulation of FoxO1 activity in high-glucose conditions. PINK1, PTEN-induced putative kinase 1; TGF-β1, transforming growth factor-beta1; ILK, integrin-linked kinase; EMT, epithelial-mesenchymal cell transformation; TIMP3, tissue inhibitors of metalloproteinase3; CAT, catalase; SOD, superoxide dismutase; MDA, malondialdehyde; ROS, reactive oxygen species; ECM, extracellular matrix; TXNIP, thioredoxin-interacting protein; TRX, thioredoxin; p-STAT1, phosphorylated STAT1.