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Endothelial cells and smooth muscle cells (SMCs) are the key elements in the pathogenesis and treatment of vascular disease. We are beginning to understand their intricate interactions. Dysfunction of arterial endothelium is the first stage of atherosclerosis, but it is the migration and proliferation of other cells (SMCs included) that forms the plaque. Our current understanding of in-stent restenosis is based on the concept of vessel wall injury, de-endothelization and the exposure of SMCs from tunica media. Endothelialization of the implant ensures healing of the intervention site. Migration of SMCs into the vessel lumen, their proliferation and secretion of the extracellular matrix are the key elements of restenosis. It is the delicate play between those two types of cells that needs to be understood and ideally also regulated in order to make the effects of intravascular interventions long-lasting.

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