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Tear film mucins are high-molecular-weight glycoproteins that are fundamental to the stability and protective function of the ocular surface (Gipson, 2004, PMID: 14967200). They are categorized into membrane-associated mucins (e.g., MUC1, MUC4, MUC16), which form the glycocalyx on the corneal and conjunctival epithelium, and gel-forming secreted mucins (primarily MUC5AC), which are produced by conjunctival goblet cells (Mantelli & Argüeso, 2008, PMID: 18554540). These mucins transform the hydrophobic ocular surface into a hydrophilic one, allowing the aqueous tear layer to spread evenly and providing a barrier against pathogens and mechanical friction. In conditions like dry eye disease, mucin production is often diminished or altered, leading to tear film instability and epithelial damage (Pflugfelder & Paiva, 2017, PMID: 28603015). Therapeutic strategies involve the use of mucin secretagogues such as diquafosol and rebamipide to restore the mucin layer, as well as anti-inflammatory agents to prevent the loss of goblet cells (Koh, 2016, PMID: 27553915).
Mucin secretagogues like diquafosol act as P2Y2 receptor agonists to stimulate mucin release from goblet cells, while rebamipide increases the expression of membrane-associated mucins; anti-inflammatory agents help maintain the health of mucin-producing cells.
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