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The ocular surface and corneal epithelium constitute the outermost anatomical boundary of the eye, serving as a critical physical and physiological barrier against environmental pathogens and mechanical trauma (StatPearls, NBK470347). The corneal epithelium is a non-keratinized, stratified squamous layer that is essential for maintaining ocular transparency and providing the majority of the eye's refractive power (NIH/NEI, Dry Eye). Dysfunction of this tissue, often characterized by inflammation and loss of tear film homeostasis, leads to ocular surface diseases such as dry eye or neurotrophic keratitis (Journal of Ocular Pharmacology and Therapeutics, 2016). While various pharmacological agents like Cyclosporine and Lifitegrast are applied to this region to treat disease, the ocular surface itself is an anatomical structure containing multiple cell types and molecular pathways rather than a single therapeutic target molecule. Consequently, drug development focuses on specific receptors, such as LFA-1 or growth factor receptors, located within these epithelial layers to restore the integrity of the ocular surface (PubMed, PMC5344495).
Drugs targeting this region typically act via immunomodulation (e.g., calcineurin inhibition), antagonism of lymphocyte function-associated antigen-1 (LFA-1), or by providing neurotrophic support through recombinant human nerve growth factor (rhNGF) to stimulate epithelial proliferation and differentiation.
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