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The endothelial glycocalyx is a complex, gel-like layer of proteoglycans, glycoproteins, and glycosaminoglycans that coats the luminal surface of the vascular endothelium (Reitsma et al., 2007). It serves as a critical physical and chemical barrier that regulates vascular permeability, prevents microvascular thrombosis, and modulates the recruitment of inflammatory cells (Weinbaum et al., 2007). Beyond its structural role, the glycocalyx acts as a mechanotransducer, sensing blood flow-induced shear stress to trigger the release of vasodilators like nitric oxide. In pathological conditions such as sepsis, trauma, and diabetes, the glycocalyx is rapidly degraded or ackslash"shedackslash" by enzymes like heparanase, leading to capillary leak, edema, and impaired organ perfusion (Uchimido et al., 2019). Therapeutic strategies focus on protecting this layer from enzymatic breakdown or replenishing its components using agents like sulodexide or albumin to restore microvascular stability (Becker et al., 2010). As a therapeutic target, the endothelial glycocalyx represents a pivotal frontier for treating systemic inflammatory syndromes and chronic vascular diseases.
Pharmacological stabilization involves inhibiting shedding enzymes such as heparanase and matrix metalloproteinases (MMPs), replenishing glycosaminoglycan constituents (e.g., heparan sulfate, hyaluronan), and maintaining the osmotic pressure of the endothelial surface layer to prevent collapse and leakage (Uchimido et al., 2019; Becker et al., 2010).
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