Influence of homocysteine on the interaction between circulating monocytes and endothelial cells
Abstract
Mild hyperhomocysteinemia is an independent risk factor for the development of coronary artery disease, cerebrovascular disease and peripheral arterial disease. The mechanisms by which hyperhomocysteinemia promotes vascular disease are not completely understood yet. An increasing body of evidence has implicated oxidative stress as being contributory to homocysteine’s deleterious effects on the vasculature. Elevated levels of homocysteine lead to increased generation of superoxide anion in endothelial cells by a biochemical mechanism involving nitric oxide synthase, and, to a lesser extent, by an increase in the chemical oxidation rate of homocysteine and other aminothiols in the circulation. Furthermore, homocysteine has been shown to inhibit the activity of important cellular antioxidant enzymes, like the cellular isoform of glutathione peroxidase or superoxide dismutase, which may contribute to homocysteine’s induced oxidant stress. The resulting increase in reactive oxygen species leads to decreased bioavailability of the endothelium-derived signaling molecule nitric oxide via oxidative inactivation and thereby induces endothelial dysfunction. This seems to play a central role in the molecular mechanisms underlying the effects of homocysteine on vascular function. Hyperhomocysteinemia not only leads to endothelial dysfunction but also promotes the development and propagation of atherosclerotic lesion in atherosclerosis-prone animal models. As the recruitment of…
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