Abstract
The endothelial glycocalyx, the gel layer covering the endothelium, is composed of glycosaminoglycans, proteoglycans, and adsorbed plasma proteins. This structure modulates vessels’ mechanotransduction, vascular permeability, and leukocyte adhesion. Thus, it regulates several physiological and pathological events. In the present review, we described the mechanisms that disturb glycocalyx stability such as reactive oxygen species, matrix metalloproteinases, and heparanase. We then focused our attention on the role of glycocalyx degradation in the induction of profibrotic events and on the possible pharmacological strategies to preserve this delicate structure.
Highlights
The endothelium was once only known as the cellular internal monolayer of blood and lymphatic vessels, but it is recognized as a dynamic organ
In the last few years, it has appeared that (1) a great deal of endothelial functions are modulated and mediated by the glycocalyx, (2) the integral endothelial surface layer is an important element in tissue homeostasis, and (3) alterations of this structure are involved in several pathophysiological conditions: sepsis as well as chronic cardiovascular, renal, and metabolic diseases [4,5,6,7]
Cell adhesion molecules on the endothelium, such as integrins and immunoglobulin glycoproteins, are hidden within the glycocalyx, but, once infection occurs, the glycocalyx is degraded by inflammatory mediators, which facilitate ligand–receptor interactions that promote the adhesion of leukocytes (Figure 1) [38]
Summary
The endothelium was once only known as the cellular internal monolayer of blood and lymphatic vessels, but it is recognized as a dynamic organ. Endothelial cell phenotype is different in different organs and districts, and this reflects specific functions [1]. Endothelial cells are covered by a gelatinous layer called the “glycocalyx”, which represents an important element of the vascular barrier [3]. In the last few years, it has appeared that (1) a great deal of endothelial functions are modulated and mediated by the glycocalyx, (2) the integral endothelial surface layer is an important element in tissue homeostasis, and (3) alterations of this structure are involved in several pathophysiological conditions: sepsis as well as chronic cardiovascular, renal, and metabolic diseases [4,5,6,7]. We will discuss the present and possible future strategies aimed at preserving this delicate structure
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