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Restenosis after endovascular interventions is a clinically relevant process that is directly associated with increased morbidity. Thereby, an increased migration and proliferation of vascular smooth muscle cells (VSMCs) is mainly responsible for recurrent lumen narrowing. Previously, we showed that caveolin‑1 (Cav‑1) and endothelial nitric oxide synthase (eNOS) were directly involved in neointimal proliferation.

Influence of caveolin-1 and endothelial nitric oxide synthase on adventitial inflammation in aortic transplants