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Concurrently, activation of the Nrf2GSH axis enhances the cellular antioxidant capacity, enabling tumor cells to maintain redox homeostasis under targeted therapyinduced oxidative stress, thus facilitating metabolic escape [77]

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for example, in sepsis or ischemia-reperfusion injuries, impaired GPx4 allows ferroptosis to contribute to tissue damage, worsening outcomes

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Prolonged exposure to stress further elevates the activity of monoamine oxidase-A (MAO-A) while concurrently diminishing monoamine biosynthesis, thereby exacerbating depressive-like manifestations (26)