Effects of statins on endothelium and their contribution to neovascularization by mobilization of endothelial progenitor cells

Statins are potent drugs with a variety of cardiovascular protective effects which appear to occur independent of cholesterol reduction. The vasculoprotective effects of statins might be due to their direct effect on endothelial cells leading to improved nitric oxide (NO) bioavailability. Mechanistically, statins induce endothelial nitric oxide synthesis (eNOS) mRNA stability in endothelial cells and promote eNOS activity through a PI3K/Akt dependent pathway. Novel targets of statins are pro-angiogenic actions including the mobilization and differentiation of bone marrow derived endothelial progenitor cells, which accelerate angiogenesis or re-endothelialization. The functional improvement and increased homing capacity of endothelial progenitor cells induced by statin treatment might reverse impaired functional regeneration capacities seen in patients with risk factors for coronary artery disease or documented active coronary artery disease.