Corneal surface protection via anti-inflammatory effect of omega‑3 fatty acids

Corneal surface protection via anti-inflammatory effect of omega‑3 fatty acids" is not a specific molecule or receptor but rather describes a **therapeutic mechanism** by which omega‑3 polyunsaturated fatty acids—primarily eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)—exert beneficial effects on the ocular surface. These effects are mediated through several biological actions: Omega‑3 supplementation has been shown to reduce inflammation on the corneal and conjunctival surfaces, decrease tear film osmolarity, improve tear break-up time, lower MMP‑9 levels, enhance meibomian gland function by altering lipid composition in secretions, and promote regeneration of the corneal nerve plexus damaged in dry eye disease. The anti-inflammatory action is thought to involve both direct modulation of inflammatory pathways and indirect effects such as increasing production of specialized pro-resolving mediators like resolvins derived from EPA/DHA. These mechanisms collectively contribute to improved symptoms and clinical signs in patients with dry eye disease or meibomian gland dysfunction.[1][2][3][4][5] Because this entry refers to a therapeutic process rather than a discrete molecular target such as a receptor or enzyme, it should not be considered an individual "target" for drug discovery purposes.

Other names

Omega-3 fatty acids (O3FAs)Eicosapentaenoic acid (EPA)Docosahexaenoic acid (DHA)

Modulation of inflammatory pathways, including competitive inhibition with omega‑6 fatty acids for desaturase enzymes, leading to reduced pro-inflammatory mediators and increased anti-inflammatory resolvins derived from EPA/DHA