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The ocular surface mucin-rich glycocalyx is a specialized extracellular layer composed primarily of membrane-associated mucins, such as MUC1, MUC4, and MUC16, along with secreted mucins like MUC5AC (Gipson, 2004). It serves as a critical hydrophilic interface that anchors the aqueous tear film to the hydrophobic corneal and conjunctival epithelium, ensuring uniform wetting and lubrication across the ocular surface (Mantelli & Argüeso, 2008). Beyond its role in lubrication, the glycocalyx acts as a robust physical and chemical barrier that excludes pathogens, prevents environmental debris from adhering to the eye, and minimizes mechanical friction during blinking (Govindarajan & Gipson, 2010). In pathological conditions such as dry eye disease (DED) and Sjögren's syndrome, the glycocalyx is often degraded or poorly formed, leading to tear film instability, epithelial damage, and chronic inflammation (Gipson, 2004). Therapeutic strategies focus on restoring this layer through mucin secretagogues like rebamipide and diquafosol, which enhance the expression and secretion of mucins to stabilize the ocular surface and alleviate symptoms (Uchino et al., 2016). Maintaining the integrity of the glycocalyx is essential for visual clarity, comfort, and the overall health of the ocular surface.
Stimulation of mucin gene expression (specifically MUC1, MUC4, and MUC16) in corneal and conjunctival epithelial cells, and induction of mucin secretion from goblet cells to restore the hydrophilic interface and stabilize the tear film (Uchino et al., 2016; Dartt, 2009).
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