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Oxidative inactivation of redox sensitive cysteine residues in Keap1, specific phosphorylation of Nrf2, or increased expression of p62, which competes with Nrf2 for Keap 1 binding, disrupts the Keap1/Nrf2 interactions to foster the stabilization and nuclear translocation of Nrf2 where it promotes transcription of a variety of protective antioxidant genes via the antioxidant response element or ARE in their promoter regions

Transfusion 55:205219

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Identification of hyperoxidized PRDX3 as a ferroptosis marker reveals ferroptotic damage in chronic liver diseases