A study of vascular wound healing in a rabbit model of type I diabetes.

The pathophysiology of restenosis following balloon catheterization involves a sequence of events similar to wound healing (1). Mechanical stress and mitogens released by cells at the site of injury activate quiescent vascular smooth muscle cells (VSMC) of the contractile phenotype to dedifferentiate to the synthetic phenotype and, subsequently, divide. Activated VSMC of the synthetic phenotype migrate through breaks in the internal elastic lamina to the intima where they continue to proliferate and synthesize abundant extracellular matrix (ECM), resulting in an increased neointimal mass. This intimal hyperplasia has been suggested to contribute to a decrease in lumen diameter and patency of the vessel resulting in ischemic symptoms. It should be noted, however, that the contribution of intimal thickening to the pathophysiology of restenosis has recently been questioned.