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In response to inflammatory stimuli, astrocytes can be activated and may adopt a reactive phenotype, characterized by the increased expression of glial fibrillary acidic protein (GFAP) and release of pro-inflammatory cytokines [132]

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However, under defined pathophysiological stresses, including inflammatory cues, metal overload, cysteine deprivation, or drug exposure, GSH oxidation and thiol chemistry may become coupled to metal redox cycling and mitochondrial damage amplification, thereby increasing susceptibility to forms of regulated cell death such as ferroptosis and cuproptosis

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