Vascular Endothelial Glycocalyx as a Mechanism of Vascular Endothelial Dysfunction and Atherosclerosis

Atherosclerosis occurs as a result of organized processes that include vascular endothelial dysfunction, lipid accumulation, abnormal inflammatory reaction, excessive reactive oxygen species production, and vascular cell proliferation and migration. In patients with atherosclerosis, vascular endothelial dysfunction is commonly observed with the damage of vascular endothelial glycocalyx, which is an extracellular matrix bound to and encapsulating the endothelial cells that line the blood vessel wall. Unhealthy lifestyle choices such as smoking and physical inactivity also induce glycocalyx degradation. Additionally, vascular endothelial glycocalyx can be damaged by various pathological conditions including dehydration, acute infectious disease, trauma, sepsis, acute respiratory distress syndrome, Kawasaki disease, preeclampsia, gestational diabetes mellitus, hypertension, diabetes mellitus, chronic kidney disease, atherosclerosis, stroke, dementia, microvascular angina, acute coronary syndrome, and heart failure. Vascular endothelial glycocalyx has been shown to be important as a physical cytoprotective barrier for vascular endothelial cells and as a regulatory mechanism for intracellular cell signaling. Therefore, vascular endothelial glycocalyx has immense potential in the exploration of novel strategies for the evaluation of beneficial conditions of healthy vasculature.