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Our findings indicated that targeting ACSL4 or, alternatively, upregulating GPX4 or FSP1 may help mitigate AKI by reducing ferroptosis, offering potential therapeutic strategies for oxalate-induced AKI
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This includes increased phosphorylation of dynamin-related protein 1 (DRP1) at serine-616, promoting mitochondrial fragmentation, and decreased expression of fusion proteins such as mitofusins (MFN1/2) and optic atrophy 1 (OPA1) (Andreazza et al., 2010
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