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The corneal epithelium relies on a specific suite of glucose transporters (GLUTs) and extracellular matrix (ECM) proteins to maintain transparency and structural integrity. GLUT1 is the predominant transporter facilitating glucose uptake from the aqueous humor to support the high metabolic activity of the epithelial layer (Takahashi et al., 1996, PMID: 8922143). The ECM, composed of proteins such as collagen type IV, laminin, and fibronectin, forms the basement membrane and provides the scaffold for epithelial cell adhesion and migration (Ljubimov & Saghizadeh, 2015, PMID: 25703250). In conditions like diabetic keratopathy, hyperglycemia leads to the downregulation of GLUTs and the thickening of the basement membrane through excessive ECM deposition, which impairs wound healing and nerve function (Kaji, 2005, PMID: 15851931). While not a single therapeutic target, this system is a focus for ocular drug delivery research, where GLUTs are exploited to transport prodrugs across the corneal barrier (Vooturi et al., 2012, PMID: 22403145). Modulating ECM components also represents a strategy for treating persistent corneal epithelial defects and scarring.
Facilitated diffusion of glucose via GLUT transporters and structural support/signaling via extracellular matrix protein interactions.
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