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Together, these findings demonstrate that, in contrast with acute exposure, chronic disruption of iron homeostasis with consequent GSH depletion remodels cellular redox homeostasis over time, inducing a state we term chronoferroptosis: a persistent ferroptotic adaptation characterized by coordinated alterations in iron-handling and antioxidant defense proteins that may represent early vulnerability to neurodegenerative pathology

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These findings support the use of retatrutide in laboratory studies examining how coordinated GLP-1R, GIPR, and GCGR activation affects hepatic metabolic regulation [5][8]