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. 2022 Aug 9;79(9):474. doi: 10.1007/s00018-022-04505-w

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© The Author(s), under exclusive licence to Springer Nature Switzerland AG 2022. Springer Nature or its licensor holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.

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Fig. 2 — TGF-β1 and the nephrotoxin cisplatin utilize distinct p53 mediated pathways to mediate progression of renal injury. TGF-β1 initiates both canonical SMAD3 and non-canonical pathways (which involves NOX mediated ATM phosphorylation and subsequent activation of p53, which then cooperates with SMAD3) to promote fibrotic genes, epithelial cell cycle arrest and epithelial-fibroblast crosstalk leading to tubulointerstitial fibrosis (red arrows). Ciplatin phosphorylates p53 via NADPH (oxidase)/ROS dependent activation of ATR/ChK kinases. Subsequent p53 dependent induction of BAX and puma lead to tubular apoptosis/necrosis and acute kidney injury (AKI), which could transition to CKD if AKI is severe or persistent (black arrows)