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Notably, in the condition of excess hemin exposure and hypoxia, our findings suggest an important contribution of the TSS pathway and its regulation by DMF for de novo cysteine synthesis and GSH generation in protecting against the oxidative and ferroptotic stresses in SCD erythroblasts

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when the liver undergoes ischemiareperfusion injury due to hyperthermia, acute kidney injury often complicates the condition, and this combined injury significantly increases patient morbidity and mortality [76]