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Conversely, MPC1 inhibition increases cell susceptibility to ferroptosis by preserving the mesenchymal properties of erPCCs, 101 indicating that MPC1 regulates ferroptosis in erPCCs through EMT

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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