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The ocular surface lipid bilayer and membrane-associated proteins form a complex physiological barrier essential for maintaining the health and clarity of the eye. The lipid bilayer, primarily the tear film lipid layer (TFLL), is a thin oily film secreted by the meibomian glands that prevents the evaporation of the underlying aqueous tears and provides a smooth optical surface (Cwiklik, 2016). Membrane-associated proteins, such as transmembrane mucins (MUC1, MUC4, MUC16) and integrins like ICAM-1, constitute the glycocalyx and mediate cell-signaling and adhesion (Mantelli & Argüeso, 2008). In conditions like dry eye disease (DED) and meibomian gland dysfunction (MGD), the integrity of this system is compromised, leading to tear film instability, hyperosmolarity, and chronic inflammation (Craig et al., 2017). Pharmacological treatments aim to stabilize the lipid layer using perfluorohexyloctane or target membrane-associated proteins like LFA-1 with lifitegrast to inhibit inflammatory pathways (Abidi et al., 2016). Additionally, secretagogues like diquafosol target membrane receptors to enhance the production of these protective components (Lau et al., 2014). Understanding this target is crucial for developing therapies that restore the ocular surface microenvironment and alleviate symptoms of ocular surface disease.
Lipid layer stabilization, LFA-1/ICAM-1 antagonism, P2Y2 receptor agonism, and immunomodulation
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