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As we specifically observed impaired GPX4 activity in IECs from the inflamed (but not uninflamed) mucosa of CD patients, it appears plausible that GPX4 deficiency is no primary defect in CD but occurs secondary to insults (likely caused by yet unidentified cellular stressors) in the inflamed mucosa

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Another study indicated that in bleomycin-induced mice, elevated Sp3 promotes the expression of ferroptosis-related proteins and markers of mitochondrial DNA (mtDNA) damage by recruiting HDAC2, thus inactivating the keap1/NRF2 signaling cascade, resulting in ferroptosis [115]