A link between smooth muscle cell death and extracellular matrix degradation during vascular atrophy

This study identifies a small number of genes regulated in two distinct models of vascular atrophy in nonhuman primates. Some are involved in degradation of extracellular matrix, cell death, or cell differentiation. The function of others is less clear, but all may be fundamental regulators of vascular atrophy and may represent future therapeutic targets. A pharmacologic therapy based on the induction of vascular atrophy of established intimal lesions in restenotic stented vessels (arteries, vein grafts, and arteriovenous fistulas) would enable treatment of only those patients that develop stenosis rather than all patients as required when prevention of neointimal hyperplasia is the strategy.