Are the mechanisms for NO-dependent vascular remodeling different from vasorelaxation in vivo?

The remodeling of blood vessels, characterized by thickening of the vessel wall attributable to neointima formation or changing of the vessel wall thickness and diameter, occurs after injury, dysfunction, or endothelial denudation, resembling the risk associated with endovascular surgery. Upon vascular injury, activated vascular smooth muscle cells (VSMCs) of local or systemic origin contribute to the remodeling processes which may eventually lead to occlusion of the blood vessel.1 Thus, understanding the molecular aspects of occlusive neointimal proliferation is desirable to promote better therapies for this disease process.