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. 2023 Sep 2;11(3):294–308. doi: 10.2478/jtim-2023-0105

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© 2023 Naiquan Liu, Dongyang Li, Dajun Liu, Ying Liu, Jing Lei, published by De Gruyter on behalf of Scholar Media Publishing

This work is licensed under the Creative Commons Attribution 4.0 International License.

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Diagram of the working model illustrating the mechanism of FOSL2 in renal fibrosis. FOSL2 was upregulated with the stimulation of UUO and TGF-β1 and facilitated SGK1 expression at the transcriptional level, leading to increased EMT and ECM deposition, which contributes to renal fibrosis. UUO: unilateral ureteral obstruction; TGF-β1: transforming growth factor-β1; EMT: epithelial–mesenchymal transition; ECM: extracellular matrix; SGK1: serum/glucocorticoid regulated kinase 1; α-SMA: α-smooth muscle actin.