Dry eye disease (DED)

Dry eye disease (DED), also known as keratoconjunctivitis sicca, is a multifactorial disorder of the ocular surface characterized by a loss of homeostasis of the tear film, accompanied by ocular symptoms such as discomfort, visual disturbance, and tear film instability (Source: StatPearls, NIH National Eye Institute). It is not a single molecular target or receptor; rather, it is a clinical condition involving inflammation, hyperosmolarity of the tear film, and damage to the ocular surface and associated neurosensory structures. The pathophysiology is often driven by a vicious cycle of inflammation where T-lymphocyte activation and cytokine release lead to further damage of the lacrimal unit and ocular surface (Source: Mayo Clinic, PubMed). Therapeutic agents are designed to break this cycle by targeting specific molecular mediators such as Integrin alpha-L/beta-2 (LFA-1) or by providing artificial lubrication and reducing tear evaporation to restore the ocular microenvironment.

Other names

Dry eye syndromeKeratoconjunctivitis siccaDysfunctional tear syndromeXerophthalmiaOcular surface disease

Pharmacological interventions for dry eye disease target various pathways: calcineurin inhibition to reduce T-cell mediated inflammation (Cyclosporine), lymphocyte-associated antigen-1 (LFA-1) antagonism to inhibit T-cell adhesion to ICAM-1 (Lifitegrast), nicotinic acetylcholine receptor agonism to stimulate natural tear production via the trigeminal parasympathetic pathway (Varenicline), and reduction of tear evaporation through semi-fluorinated alkanes (Perfluorohexyloctane).