Vascular Remodeling in Diabetes

Diabetes mellitus is associated with increased risk of cardiovascular disease. A widespread endothelial dysfunction, altered production of vasoactive substances and superoxide and modification of the basement membranes, is believed to play a decisive role in the vascular complications observed in diabetes.1 More importantly perhaps, in diabetic patients collateral vessel development after vascular occlusion is impaired. It seems that in these patients, arteriogenesis, the growing of preexisting arteriolar connections into collateral to restore the blood supply to the ischemic area, is severely affected.2,3 This process of active vascular remodeling involves the recruitment of circulating monocytes-macrophage subsets that have a strong angiogenic response. Although these circulating angiogenic cells (CAC) do not adopt a typical endothelial phenotype in vitro, they are capable of enhancing neovascularization in a paracrine manner in vivo and are critical regulators of wound healing and tissue regeneration.4 Extensive studies have shown that the numbers of circulating angiogenic cells are significantly lower in type II diabetes, and their angiogenic potential is also dramatically diminished. These cells display defective adhesion to the endothelium, reduced proliferation rate, and impaired ability to create new vascular structures.5–7 Thus, to pursue any …