Key result
HMG-CoA reductase inhibitors (statins) exert multiple beneficial endothelium-mediated vasoactive, antithrombotic, antiproliferative, and anti-inflammatory effects in atherosclerosis.
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Endothelial dysfunction is an early event in atherosclerosis and could be considered a response to the injury induced by major risk factors. There is evidence that endothelial dysfunction is intimately involved in the onset and the progression of cardiovascular disease through abnormalities in the production, release or degradation of endothelium-derived factors, mainly nitric oxide and endothelin 1. Several reports have shown that drugs of the statin class could have multiple beneficial effects related to endothelium-mediated vasoactive, antithrombotic, antiproliferative and anti-inflammatory actions. Thus, the question arises of whether endothelial cells are the main target of statin therapy, in the setting of both hypercholesterolemia and normocholesterolemia. Experimental and clinical studies are reported that could support this hypothesis.
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Puddu et al. (2001) conducted a review in Endothelial dysfunction and atherosclerosis (hypercholesterolemia and normocholesterolemia). HMG-CoA reductase inhibitors (statins) was evaluated on Endothelium-mediated vasoactive, antithrombotic, antiproliferative, and anti-inflammatory actions. HMG-CoA reductase inhibitors (statins) exert multiple beneficial endothelium-mediated vasoactive, antithrombotic, antiproliferative, and anti-inflammatory effects in atherosclerosis.
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