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Under hyperglycemic conditions, RGCs exhibit significant mitochondrial impairment, including cristae dissolution, swelling, vacuolar degeneration, elevated reactive oxygen species (ROS) production, and diminished mitochondrial membrane potential (MMP) [68, 69]

J., Krummenacher, C., Cohen, G

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However, approximately one week postinjury, a shift in the microglial phenotype occurs at the damage site, resulting in reduced phagocytosis and increased production of proinflammatory cytokines and chemokines, as well as the recruitment of other immune populations [151, 152]

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