<p>Glaucoma is increasingly conceptualized as a chronic neurodegenerative disorder in which retinal ganglion cell loss cannot be fully attributed to intraocular pressure dependent mechanisms alone. Mounting evidence implicates dysfunction of the neurovascular unit, with astrocytes playing a central role through their neurochemical regulation of vascular tone, metabolic coupling, and redox homeostasis. Under physiological conditions, astrocytes mediate neurovascular coupling via calcium dependent signalling and controlled release of vasoactive and metabolic mediators, ensuring alignment between neuronal energy demand and local perfusion. In glaucoma, mechanical strain, ischemia, and oxidative stress induce reactive astrogliosis, leading to altered calcium dynamics, impaired nitric oxide signalling, and enhanced endothelin-driven vasoconstriction. These changes promote neurovascular uncoupling, chronic hypo perfusion, and sustained metabolic stress within the optic nerve head, even in the presence of controlled intraocular pressure. In parallel, inflammation-associated downregulation of connexin-43 disrupts astrocytic syncytial networks, impairing glutamate clearance, potassium buffering, and metabolic substrate redistribution, thereby amplifying excitotoxic and oxidative injury. Emerging transcriptomic data further demonstrate astrocyte heterogeneity, with distinct neurochemical phenotypes exerting either protective or neurotoxic effects. Collectively, these findings position astrocytic neurochemical dysfunction as a key driver of glaucomatous neurodegeneration and identify glial signalling pathways as rational targets for disease-modifying intervention.</p>