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Nathan BM, Rudser KD, Abuzzahab MJ, Fox CK, Coombes BJ, Bomberg EM, et al

Gronda, Glucagon and heart in type 2 diabetes: new perspectives, Cardiovasc

& Mason, P

This upregulation exhausts intracellular GSH, leading to ROS buildup and oxidative DNA damage that can ultimately generate TP53 mutations, a process that is halted when CHAC1 is knocked down ( TP53 induces ferroptosis primarily by transcriptionally repressing the expression of SLC7A11 ( TP53 lead to a loss of this repression, resulting in sustained SLC7A11 activity and greater cellular resistance to ferroptosis ( 3 KR, which cannot induce cell-cycle arrest, senescence or apoptosis, fully retains the ability to suppress SLC7A11 and trigger ferroptosis under oxidative stress ( The reasons for variable expression of CHAC1 in different cancers are still unclear, but it appears to be critically dependent on TP53 status

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