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A specific oxidoreductase, previously known as apoptosis-inducing-factor mitochondrial-2 (AIFM2), capable of recycling reduced ubiquinol (Co-enzymeQ 10 H 2 ) from ubiquinone at the expense of NAD(P)H, has been presented as a potential ferroptosis inhibitor due to the fact that its overexpression complements the loss of GPx4 in PFA1 and human fibrosarcoma (66, 67)

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Cardiac MTs also show more effects in other processes that regulate gene expression