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The ocular surface mucins and epithelial glycocalyx constitute a critical protective interface between the ocular surface and the external environment (Gipson, 2004, PMID: 14709590). This complex layer consists of membrane-associated mucins, such as MUC1, MUC4, and MUC16, which form the glycocalyx on corneal and conjunctival epithelial cells, as well as secreted mucins like MUC5AC produced by goblet cells (Mantelli & Argüeso, 2008, PMID: 18565258). These glycoproteins are essential for maintaining tear film stability, providing lubrication, and acting as a physical and chemical barrier against pathogens and environmental insults (Govindarajan & Gipson, 2010, PMID: 20445104). In conditions like dry eye disease, the expression and glycosylation of these mucins are often altered, leading to tear film instability and epithelial damage (Argüeso et al., 2003, PMID: 12871490). Therapeutic strategies focus on mucin secretagogues, such as diquafosol and rebamipide, which aim to restore the density and function of this layer to alleviate symptoms and promote ocular surface healing (Koh, 2016, PMID: 27553913). Restoration of the glycocalyx is also vital for preventing bacterial adhesion and maintaining the refractive properties of the cornea.
Drugs targeting this system act as mucin secretagogues (e.g., Diquafosol via P2Y2 receptor agonism) or by increasing the expression of membrane-associated mucins and goblet cell density (e.g., Rebamipide), thereby stabilizing the tear film and restoring the ocular surface barrier (Koh, 2016, PMID: 27553913; Urashima et al., 2004, PMID: 15542045).
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