Getting Neointimal

Abstract

See related articles, pages 380–387 Blood vessels are highly active structures whose morphology rapidly adapts to maintain vascular function under altered systemic and local conditions. In some instances, this normally beneficial adaptation may be detrimental to overall function. Structural adaptations with important physiological and pathophysiological impact include angiogenesis, the remodeling of resistance arteries, and stenosis and restenosis of conduit arteries. It is highly probable that the development of these diverse phenotypes involves common pathways; therefore, the vascular research field must prioritize investigating the mechanisms relevant for determining vascular structure. Remodeling of the vascular wall requires a highly dynamic and adaptable extracellular matrix (ECM). Heparan sulfate proteoglycans (HSPGs) are prominently expressed in the vascular ECM.1 HSPGs whether bound to the membranes or free in the ECM provide an extracellular storage function for a number of biologically important molecules: the heparan sulfate moieties bind ECM structural proteins and several growth factors and cytokines enabling retention of these factors in the ECM and preventing degradation of them (Figure). The HSPGs also directly transfer information from the extracellular space to intracellular kinases and cytoskeletal elements and thus modify cell adhesion and motility.2 In addition, HSPGs bind lipoprotein lipase to the endothelial cell surface.3 Thus HSPGs are important for vascular health and disease through many different pathways, and how these molecules are regulated is of considerable interest. Figure. A, Baker et al6 suggest that heparanase activation after stent placement …