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The ocular surface mucin layer and tear film constitute a complex, multi-layered fluid system essential for maintaining the health and optical clarity of the eye (Craig et al., 2017). This system is traditionally described as having three components: an outer lipid layer that prevents evaporation, a middle aqueous layer containing nutrients and antimicrobial proteins, and an inner mucin layer (glycocalyx) that anchors the tear film to the hydrophobic corneal epithelium (Gipson, 2004). Mucins, such as MUC1, MUC4, MUC16, and the secreted MUC5AC, play a pivotal role in lubrication, hydration, and providing a barrier against pathogens and environmental debris (Mantelli & Argüeso, 2008). Dysfunction or deficiency in any of these components leads to dry eye disease (DED), characterized by tear film instability, hyperosmolarity, and ocular surface inflammation (TFOS DEWS II, 2017). Therapeutic strategies targeting this system include the use of mucin secretagogues like rebamipide and diquafosol, which enhance the production of protective glycoproteins (Lau et al., 2014). Additionally, anti-inflammatory agents like cyclosporine and lifitegrast are employed to stabilize the tear film and restore the homeostatic environment of the ocular surface by preventing goblet cell loss (Pflugfelder & Stern, 2020).
Stimulation of mucin secretion from goblet cells and corneal/conjunctival epithelia; stabilization of the tear film lipid layer; reduction of surface tension; anti-inflammatory modulation to prevent goblet cell loss (Lau et al., 2014; Pflugfelder & Stern, 2020).
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