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We suggest that reduced GPx1 in monocytes recruited to the gut and intestinal macrophages renders these cells vulnerable to reactive oxygen species-evoked ferroptosis cell death and that unraveling the participation of this pathway in Crohns disease may reveal novel therapeutic approaches to this chronic condition

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This consideration becomes less relevant as patients gain confidence and experience with self-administration

DNA-binding assays have proved that p53 positively regulates an upstream promoter element of the GPX1 gene

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