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The ocular surface epithelial and goblet cell mucin pathways are essential for maintaining the integrity and stability of the tear film (Mantelli & Argüeso, 2008). These pathways involve the synthesis and secretion of membrane-associated mucins (MUC1, MUC4, MUC16) by corneal and conjunctival epithelial cells, which form the protective glycocalyx, and the secretion of gel-forming mucins (MUC5AC) by conjunctival goblet cells (Dartt, 2004). Together, these mucins provide lubrication, retain moisture, and serve as a barrier against pathogens and environmental stressors (Watanabe, 2002). Dysregulation of these pathways, often manifesting as decreased mucin production or goblet cell loss, is a primary feature of dry eye disease and Sjögren's syndrome (Baudouin et al., 2019). Therapeutic interventions target these pathways using secretagogues like diquafosol, which activates P2Y2 receptors to trigger mucin release, or agents like rebamipide that enhance mucin gene expression. Restoring these pathways is a key strategy for improving ocular surface health and patient comfort in chronic ocular surface diseases.
Stimulation of P2Y2 receptors to trigger mucin secretion from goblet cells and upregulation of mucin gene expression (MUC1, MUC4, MUC16, MUC5AC) in epithelial and goblet cells.
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