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Herein, we have demonstrated that CoNPs could induce the ferroptosis-like cell death through the enhancement of intracellular reactive oxygen species (ROS) level, cytoplasmic Fe 2+ level, lipid peroxidation, and consumption of reduced glutathione (GSH) as well as inhibition of glutathione peroxidase 4 (GPX4) activity

Furthermore, the Trx system mediates crossregulation between autophagy and ferroptosis, as well as autophagy and apoptosis, thereby influencing cellular responses to stress conditions

doi: 10.1016/j.arr.2022.101635 23 HarpseNGAndersenLPGgenurIRosenbergJ