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The corneal epithelial surface mucin layer is a specialized glycocalyx primarily composed of membrane-associated mucins, including MUC1, MUC4, and MUC16, which are expressed by the apical membranes of the corneal and conjunctival epithelia (Gipson, 2004; Mantelli & Argüeso, 2008). This layer acts as a vital hydrophilic interface that stabilizes the tear film, provides essential lubrication for eyelid movement, and serves as a robust physical and chemical barrier against pathogens and environmental debris (Govindarajan & Gipson, 2010). In pathological states such as dry eye disease (DED) and Sjögren's syndrome, the expression and glycosylation patterns of these mucins are significantly altered, leading to tear film instability, increased friction, and epithelial damage (Argüeso et al., 2003). Therapeutic interventions target this layer either by stimulating the endogenous production and secretion of mucins using secretagogues like diquafosol and rebamipide or by utilizing mucin-mimetic polymers to supplement the ocular surface (Fujihara et al., 2002; Urashima et al., 2004). Restoring the integrity of the mucin layer is a primary goal in treating ocular surface disorders to alleviate symptoms and prevent long-term corneal complications.
Stimulation of mucin secretion via P2Y2 receptor agonism, induction of mucin gene expression (MUC1, MUC4, MUC16), or anti-inflammatory action to restore goblet cell density and glycocalyx integrity.
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