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Ocular surface mucins are a group of high-molecular-weight glycoproteins that constitute the innermost layer of the tear film, essential for maintaining the health and integrity of the corneal and conjunctival epithelia (Gipson, 2004). These mucins are categorized into membrane-associated forms (such as MUC1, MUC4, and MUC16), which form the glycocalyx, and secreted gel-forming forms (primarily MUC5AC), which are produced by conjunctival goblet cells (Mantelli & Argüeso, 2008). Their primary biological role is to provide a hydrophilic interface that stabilizes the aqueous layer of the tear film, reduces friction during blinking, and acts as a physical and chemical barrier against pathogens and environmental insults (Dartt, 2002). In pathological conditions like dry eye disease, a deficiency or alteration in mucin expression leads to tear film instability, epithelial damage, and chronic inflammation (Uchino et al., 2018). Therapeutic strategies focus on enhancing mucin production through secretagogues like rebamipide and diquafosol or providing symptomatic relief through mucin-mimetic agents that restore the lubricating properties of the ocular surface (Kinoshita et al., 2013). Understanding the regulation of these mucins is critical for developing targeted treatments for various ocular surface disorders.
Drugs targeting ocular surface mucins primarily act as secretagogues to stimulate the production and secretion of mucins from goblet cells and corneal/conjunctival epithelia, or as mucin-mimetics that supplement the mucous layer to restore tear film stability and lubricity (Kinoshita et al., 2013; Dartt, 2002).
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