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Timpanaro, T
These two states are important metabolites that maintain intracellular redox homeostasis and inhibit cell ferroptosis [37, 38]
One possible explanation is that the free iron in cells cannot be directly discharged out of cells in the form of ferric iron, but relies on ceruloplasmin and hephaestin to catalyze ferrous iron into ferric iron [59, 60]
Thus, we can conclude that erastin-induced ESC ferroptosis in turn induced the secretion of angiogenic, inflammatory, and growth factors, which may be associated with angiogenesis and the progression of ectopic lesions
