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& Dvorak, M

it has a systemic reach

This increase in ROS triggers mitochondrial dysfunction, further exacerbating oxidative stress and promoting cell death through both necroptosis and ferroptosis pathways (Figure 5) (Chen M.-S

Similarly, while chemically-induced accumulation of cellular ROS and lipid peroxides is strongly abrogated by joint treatment with 4-OH-E 1 (a noncovalent PDI inhibitor), it only has a weak effect on cellular NO accumulation, which is different from its abrogation of erastin-induced NO accumulation as observed in our earlier study [49]