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iNOS dimerization then leads to the accumulation of cellular NO, which subsequently results in the accumulation of cellular ROS and lipid peroxides as well as mitochondrial ROS and lipid peroxides, and ultimately, oxidative ferroptosis

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ROS can be regulated by glutathione peroxidases (GPxs), which are the key enzymes that maintain ROS homeostasis in vivo through the reduction of ROS [10]

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In addition, a moderately augmented level of ROS induces the expression of genes coding for these antioxidant enzymes and redox-regulated chaperones 12