Abstract
Dry eye (DE) is a multifactorial ocular surface disease characterized primarily by tear film instability and ocular discomfort. Nearly all forms of DE exhibit elevated inflammatory markers in tear fluid, accompanied by clinical signs of tear dysfunction including reduced secretion and shortened breakup time. Although the pathophysiology of dry eye disease remains incompletely understood, accumulating evidence implicates neutrophil extracellular traps (NETs) as key pathogenic drivers. Robust clinical associations and mechanistic studies have established causal links between NETs and ocular surface pathology. This review summarizes current research on the role of NETs in the development of dry eye, aiming to identify potential therapeutic targets.