Endothelial arginase: A new target in atherosclerosis

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Abstract
Decreased endothelial nitric oxide (NO) bioavailability as it relates to endothelial dysfunction plays an important role in various cardiovascular disorders, including atherosclerosis. 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 enzymatic activity, which contributes to the increased oxidative stress in atherosclerosis. Among other mechanisms, the substrate L-arginine is an important limiting factor for NO production. Emerging evidence demonstrates that L-arginine is not only converted to NO via eNOS, but also metabolized to urea and L-ornithine via arginase in endothelial cells. Hence, arginase competes with eNOS for the substrate L-arginine, resulting in deceased NO production. There are an increasing number of studies showing that enhanced arginase gene expression and/or activity contribute to endothelial dysfunction in various cardiovascular disorders, including atherosclerosis. Thus, endothelial arginase may represent a new therapeutic target in atherosclerosis.

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