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As ferroptosis is driven by lipid peroxidation and oxidative stress, xCT sustains glioblastoma survival by maintaining intracellular cysteine levels, which serve as a precursor for GSH synthesis, a key antioxidant that mitigates ROS-induced lipid peroxidation [49,50,51]

Ferroptosis induction was coupled to an increase in turnover of LC3B and autophagosome formation, consistent with the notion that lipid peroxidation as well as oxidized lipids could promote autophagy activation [63]