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Abstract Our recent studies have demonstrated that aspirin treatment prevents inflammatory and oxidative stress-induced alterations in mitochondrial function, improves glucose tolerance and pancreatic endocrine function and preserves tissue-specific glutathione (GSH)-dependent redox homeostasis in Goto-Kakizaki (GK) diabetic rats

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579 In addition, metabolic disorders of neuronal Ca 2+ can drive ferroptosis through interactions with iron and crosstalk between the ER and mitochondria, and maintaining Ca 2+ homeostasis to inhibit ferroptosis may be an innovative target for the treatment of AD