Smoking and cardiovascular disease: mechanisms of endothelial dysfunction and early atherogenesis.

摘要: Smoking represents one of the most important preventable risk factors for development atherosclerosis. The present review aims at providing a comprehensive summary published data from clinical and animal studies, as well results basic research on proatherogenic effect smoking. Extensive search literature revealed vast amount influence cigarette smoke its constituents early atherogenesis, particularly endothelial cells. Vascular dysfunction induced by smoking is initiated reduced nitric oxide (NO) bioavailability further increased expression adhesion molecules subsequent dysfunction. Smoking-induced adherence platelets macrophages provokes procoagulant inflammatory environment. After transendothelial migration activation, take up oxidized lipoproteins arising oxidative modifications transdifferentiate into foam In addition to direct physical damage cells, induces tissue remodeling, prothrombotic processes together with activation systemic signals, all which contribute atherogenic vessel wall changes. There are still great gaps in our knowledge about effects cardiovascular disease. However, we know that cessation effective measure reversing has already occurred preventing fatal outcomes.