Table 2.

This table summarizes the role of the GCX in endothelium function, in blood vessel health or disease, and as a potential therapeutic target

Atherosclerosis	• Most common precursor to cardiovascular diseases such as strokes and myocardial infarctions • Initiated by excessive accumulation of LDLs in luminal region of blood vessel walls • Disturbed flow regions of vessel bifurcations atheroprone, with degraded or compromised GCX in these regions
GCX structure and location	• Negatively charged heterogeneous polysaccharide that lines the luminal wall of blood vessels • Primarily consists of heparan sulfate, hyaluronic acid, sialic acid, and chondroitin sulfate
GCX-mediated endothelium functions
Barrier Function	• GCX acts as a barrier between the blood and vessel walls, filtering small molecules, lipoproteins, and circulating blood cells that seek to permeate vessel walls • A degraded or collapsed GCX has been shown to increase permeability of molecules and inflammatory cells • Healthy GCX reduces permeability
Cell-to-cell communication	• GCX attached to endothelial cell cytoskeleton which has a link to communicating gap junctions • Degraded GCX showed a decrease in gap junction protein (connexin) expression as well as communication activity
Vascular tone	• GCX has a role in the production of vasodilatory factor nitric oxide • eNOS, the enzyme that produces nitric oxide, can be significantly decreased by non-uniform flow and/or when GCX is also degraded
Standard atherosclerosis treatment options	• Statins (lipid lowering therapy) • Aspirin (anti-platelet therapy)
GCX as therapeutic	• Strengthening the GCX to counteract its degradation can restore barrier function, cell-to-cell communication, and vascular tone • Viable preventative and treatment option for addressing atherosclerosis