Abstract

The innermost layer of a normal blood vessel wall, the tunica intima, consists of a simple monolayer of endothelial cells seated on a basement membrane. Expansion of the intima is a common characteristic of atherosclerosis, restenosis after angioplasty, late closure of saphenous vein grafts and transplant vascular disease. The intima becomes a complex connective tissue containing vascular smooth muscle cells that have invaded from the underlying tunica media and inflammatory cells that have invaded from the circulation. This brief review will concentrate on the molecular events underlying the generation of this neointima ‘in response to injury’ and its consequences for disease. It will also consider the implications for the consequences and early detection of vascular drug toxicity.

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