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Concurrently, mitochondrial ROS (mtROS) amplifies vascular dysfunction by oxidizing BH4, uncoupling endothelial eNOS, and reducing NO bioavailability while also activating pro-inflammatory pathways (e.g., NLRP3 inflammasome) and stimulating NOX activity, creating continuous oxidative damage (Penna and Pagliaro, 2025)
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Activation of PI3K/Akt/mTOR signalling, or prevention of its inhibition by ethanol and related stressors, supports neuronal survival, autophagic clearance of damaged proteins and metabolic resilience [7,66,96]
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