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The **ocular surface mucous layer** is not a single molecular target but rather refers to one component of the multilayered tear film that covers the cornea and conjunctiva. This **mucous/mucin-rich layer** is primarily composed of high-molecular-weight glycoproteins called **mucins**, which are secreted mainly by goblet cells in the conjunctiva as well as some epithelial cells. The main secreted gel-forming mucin on the ocular surface is **MUC5AC**, while membrane-associated mucins such as MUC1, MUC4, and MUC16 form part of the glycocalyx on epithelial surfaces. The mucus layer plays critical roles in maintaining hydration/wettability, providing lubrication during blinking, forming a barrier against pathogens/foreign bodies, stabilizing the tear film so it adheres evenly across the eye’s front surface, smoothing optical irregularities for clear vision, and protecting underlying tissues from environmental insults.\n\nDeficiency or dysfunction in this mucus/mucin system—such as reduced numbers/activity of goblet cells or altered expression/secretion—can contribute significantly to dry eye disease and other ocular-surface disorders. Some drugs used clinically aim to stimulate production/secretion/integrity of this protective mucus barrier through indirect mechanisms such as activating P2Y₂ receptors with diquafosol or increasing goblet cell numbers with rebamipide.\n\nBecause "ocular surface/mucous layer" describes an anatomical/functional region rather than a discrete protein/receptor/enzyme/transporter/etc., it should not be considered a canonical therapeutic target at the molecular level.[1][2][3]
Stimulation of mucin secretion from conjunctival goblet cells (e.g., by diquafosol via P2Y₂ receptor activation)[6]; Increase in goblet cell number and mucin production (e.g., by rebamipide)[6]
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