Abstract
Arginase in the vascular endothelium: friend or foe?
Highlights
Arginase in the vascular endothelium and stresses the need for alternative strategies to inhibit arginase
Since both arginase isoforms are expressed in vascular endothelial cells, they can potentially interfere with the activity of endothelial nitric oxide synthase, by “stealing away” the common substrate l-arginine, required to generate nitric oxide (NO) and l-citrulline
A pathological increase in vascular arginase activity was shown to significantly contribute to “endothelial nitric oxide synthase (eNOS) uncoupling,” a phenomenon observed in various vascular pathologies and in aging [16], during which the enzyme generates detrimental amounts of superoxide instead of the vasoprotective NO
Summary
Arginase in the vascular endothelium and stresses the need for alternative strategies to inhibit arginase. This special issue, entitled “the role of arginase in endothelial dysfunction,” assembles original contributions [1,2,3,4], as well as timely reviews [5,6,7,8,9,10,11,12] broadly related to the deleterious activities of the manganese-containing enzyme arginase in the vascular endothelium. Since both arginase isoforms are expressed in vascular endothelial cells, they can potentially interfere with the activity of endothelial nitric oxide synthase (eNOS), by “stealing away” the common substrate l-arginine, required to generate nitric oxide (NO) and l-citrulline.
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