In: Basic Research in Cardiology, 2005, vol. 100, no. 2, p. 102-111
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In: Cardiovascular Research, 2011, vol. 89, no. 3, p. 485-486
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In: Frontiers in Inflammation, 2013, vol. 4, p. 149
Oxidative stress and inflammation in the vascular wall are essential mechanisms of atherosclerosis and vascular dysfunctions associated with risk factors such as metabolic diseases, aging, hypertension, etc. Evidence has been provided that activation of the vascular endothelial cells in the presence of the risk factors promotes oxidative stress and vascular inflammatory responses, leading to...
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In: Current Hypertension Reports, 2006, vol. 8, no. 1, p. 54-59
Decreased endothelial nitric oxide (NO) bioavailability as it relates to endothelial dysfunction plays an important role in various cardiovascular disorders, including atheroÂsclerosis. Recent research has provided evidence that endothelial dysfunction in atherosclerosis is not primarily caused by decreased endothelial NO synthase (eNOS) gene expression, but rather deregulation of eNOS...
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In: Basic Research in Cardiology, 2005, vol. 100(2), p. 102
Nitric oxide (NO) and monocyte chemoattractant protein–1 (MCP-1) exert partly opposing effects in vascular biology. NO plays pleiotropic vasoprotective roles including vasodilation and inhibition of platelet aggregation, smooth muscle cell proliferation, and endothelial monocyte adhesion, the last effect being mediated by MCP–1 downregulation. Early stages of arteriosclerosis are associated...
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In: Circulation, 2004, vol. 110, p. 3708-3714
Background— Arginase competes with endothelial nitric oxide synthase (eNOS) for the substrate L-arginine and decreases NO production. This study investigated regulatory mechanisms of arginase activity in endothelial cells and its role in atherosclerosis. Methods and Results— In human endothelial cells isolated from umbilical veins, thrombin concentration- and time-dependently stimulated...
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