Atherosclerosis, an inflammatory-driven disease, is characterized by the accumulation of cholesterol in arterial blood vessels, resulting in thicker and more fragile artery vessels. Binding of low-density lipoprotein (LDL) to GAGs is considered to be one of the steps in the onset of this disease 54. The GAG interaction enhances LDL uptake by macrophages, leading to the formation of foam cells (Fig. 4C). IdoA both in CS/DS and heparan sulfate is reported to enhance the binding of VLDL and LDL 55,56. Recently, it was reported that an antibody against CS/DS inhibited the LDL–CS/DS interaction and inhibited LDL oxidation in vitro 57. Furthermore, the injection of anti-CS/DS antibody in an atherosclerosis model of ApoE−/− mice resulted in decreased arteriosclerotic lesions 58.
