Fig. 9. FTO inhibits DOX-induced ferroptosis by activating P53–P21/Nrf2 in a HuR-dependent m6A manner. Mechanistically, DOX-induced cardiotoxicity was associated with inhibition of FTO. FTO overexpression mediates m6A demethylation of P53, which is up-stream of P21. In addition, FTO also activateS P21/Nrf2 by mediating their mRNA m6A demethylation directly. P21/Nrf2 signaling is important for the anti-ferroptosis effect of FTO. HuR is crucial for FTO-mediated regulations of ferroptosis and P53–P21/Nrf2 by binding with their mRNAs and enhancing their stability. Moreover, P21 in turn, decreased the expression of HuR and P53 and HuR also up-regulated the expression of FTO, suggesting that there is a positive feedback loop for P53–P21.
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