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Background Loss of endothelial NO production after arterial injury may contribute to restenosis,characterized by neointima formation and elastic recoil.Previous studies have established that bone marrow-derived endothelial progenitor cells (EPCs) play an important role in vascular repair.In this study,we investigated that hypothesis that overexpression of vasculoprotective gene endothelial nitric oxide synthase (eNOS) in EPCs may restore NO production and inhibit neointimal hyperplasia.