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The interaction between ferroptosis and inflammatory signaling pathways

Novel insights into redox system and the mechanism of redox regulation

It has been demonstrated that the TP53 gene, located on chromosome 17, contributes to the maintenance of mitochondrial integrity, and that TP53 deficiency can be compensated for by an increase in aerobic glycolysis and an enhancement of mitochondrial mass ( One of the biological effects of CB-839 is the inhibition of glutathione synthesis due to the depletion of glutamate as the pivotal precursor for glutathione synthesis

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In contrast, iron supplementation had no significant impact on lesion progression in this model, likely due to the intrinsic resistance of EMS lesions to iron overload-induced ferroptosis