Redox-inflammation pathways in ocular disease: Targets for nutritional modulation

Abstract

Visual impairment remains a major global health burden caused by diverse ocular diseases, including age-related macular degeneration, diabetic retinopathy, glaucoma, uveitis, and ocular surface disorders. Despite differing etiologies, growing evidence identifies oxidative stress and chronic inflammation as a shared pathogenic axis affecting both anterior and posterior ocular segments. High metabolic demand, sustained light exposure, dense mitochondrial content, and limited antioxidant defences render ocular tissues particularly susceptible to redox imbalance. Excess reactive oxygen species induce cellular injury and activate redox-sensitive inflammatory signalling, promoting neurodegeneration, microvascular dysfunction, immune-mediated damage, and progressive vision loss. This review summarises key mechanisms underlying redox–inflammatory crosstalk in ocular tissues, highlighting mitochondrial dysfunction, Nrf2–Keap1 antioxidant responses, NF-κB-driven inflammation, and MAPK and PI3K–Akt signalling as central molecular integrators. Tissue-specific responses in the retina, retinal pigment epithelium, trabecular meshwork, uveal tract, and ocular surface demonstrate how shared mechanisms generate distinct disease phenotypes. The modulatory potential of bioactive nutrients, including omega-3 fatty acids, carotenoids, and polyphenols, is critically discussed. Although preclinical evidence is strong, clinical outcomes remain variable, underscoring the need for precision nutrition strategies and mechanism-based clinical trial design.