Observational study shows glucose metabolism alleviates retinal cell senescence, indicating a potential strategy for age-related degeneration.
Glucose metabolic reprogramming mediates iron-induced RPE senescence, with transient glucose flux surge driving pathology via ROS-related mitochondrial damage. Targeting glucose metabolism may preserve mitochondria homeostasis and prevent RPE degeneration in age-related macular degeneration.
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Zhao et al. (2026) studied this question.
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