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Circ Res. 2008 Apr 25;102(8):923-32. doi: 10.1161/CIRCRESAHA.107.169573. Epub 2008 Feb 28.

Endothelial arginase II: a novel target for the treatment of atherosclerosis.

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  • 1Department of Anesthesiology/Critical Care Medicine, the Johns Hopkins Medical Institutions, Baltimore, MD 21287, USA.


Oxidized low-density lipoproteins increase arginase activity and reciprocally decrease endothelial NO in human aortic endothelial cells. Here, we demonstrate that vascular endothelial arginase activity is increased in atherogenic-prone apolipoprotein E-null (ApoE(-/-)) and wild-type mice fed a high cholesterol diet. In ApoE(-/-) mice, selective arginase II inhibition or deletion of the arginase II gene (Arg II(-/-) mice) prevents high-cholesterol diet-dependent decreases in vascular NO production, decreases endothelial reactive oxygen species production, restores endothelial function, and prevents oxidized low-density lipoprotein-dependent increases in vascular stiffness. Furthermore, arginase inhibition significantly decreases plaque burden. These data indicate that arginase II plays a critical role in the pathophysiology of cholesterol-mediated endothelial dysfunction and represents a novel target for therapy in atherosclerosis.

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