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Conclusions Ischemic stroke triggers a coordinated metabolic crisis characterized by ATP depletion, mitochondrial dysfunction, excitotoxicity, oxidative and nitrosative stress, maladaptive glycolysis, lactate and pH dysregulation, NAD + /FAD imbalance, inflammatory immunometabolism, endothelial-pericyte uncoupling, and impaired neurovascular repair
24,25 In this review, we provide a comprehensive overview of EC, emphasizing recent progress in epidemiology, molecular pathogenesis, and clinical management
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