Arginase as a Critical Prooxidant Mediator in the Binomial Endothelial Dysfunction-Atherosclerosis

Figure 2

Role of arginase isoforms in nitric oxide metabolism in the vasculature. The complex web of interactions among circulating factors, membrane receptors, and intracellular signaling pathways directly interferes with vascular homeostasis. The balance between the activities of the endothelial nitric oxide synthase and the arginase isoforms is critical for maintaining the adequate nitric oxide bioavailability. Once the imbalance is established, either for increased reactive oxygen species production, decreased nitric oxide availability, or both, the phenomenon of endothelial dysfunction (in this figure represented by endothelial cells in yellow) may occur, being the initial event in the establishment and progression of atherosclerosis. As a consequence of such vascular damage, the arterial impairment progresses, increasing the risk of developing different atherosclerotic events, among which are stroke (1), myocardial infarction (2), and peripheral artery disease (3).