In the classical ferroptosis regulatory pathway, GSH is depleted by erastin or other system Xc- inhibitors, which reduces cysteine synthesis and leads to GSH synthesis disorder [2, 72, 73]
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432 High p53 activity reduces the transcription of SLC7A11 and the antioxidant potential of frataxin-deficient cells, therefore, inhibiting P53 activity to improve system Xc and GSH content may be a potential therapeutic strategy to combat oxidative stress and possible ferroptosis in Friedreichs Ataxia
