Abstract
Coronary artery disease (CAD) remains the leading cause of death in the Western societies. Diabetes mellitus (DM) is one of the highly prevalent diseases, which remarkably accelerates the development of CAD. Experimental evidence indicates that decreased bioavailability of coronary endothelial nitric oxide (NO) contributes to the development of CAD in DM. There are recent studies showing that a selective impairment of NO synthesis occurs in coronary arteries of DM patients, which is mainly due to the limited availability of endothelial NO synthase (eNOS) precursor, l-arginine. Importantly, these studies demonstrated that DM, independent of the presence of CAD, leads to selective up-regulation of arginase-1. Arginase-1 seems to play an important role in limiting l-arginine availability in the close proximity of eNOS in vessels of DM patients. This brief review examines recent clinical studies demonstrating the pathological role of vascular arginase-1 in human diabetes. Whether arginase-1, which is crucial in the synthesis of various fundamental polyamines in the body, will represent a potent therapeutic target for prevention of DM-associated CAD is still debated.
Highlights
Coronary artery disease (CAD) remains the leading cause of death in the Western societies
The underlying mechanism(s) of CAD remain incompletely understood in human diabetes, so that effective preventive therapeutic strategies cannot be adopted in diabetic patients
Nemes et al have demonstrated that patients with type 2 diabetes exhibit a reduced coronary flow-reserve [2], a condition, which was found to be associated with increased incidence of future ischemic episode in the heart of diabetic patients [3]
Summary
Coronary artery disease (CAD) remains the leading cause of death in the Western societies. This and other studies concluded that diabetes is associated with impaired dilator function of coronary arteries and this is manifested as a reduced vasodilator or even vasoconstrictor responses [8,9,10]. Previous studies have shown that animals with experimental insulin resistance and diabetes exhibit a reduced NO-mediated, agonist-induced dilation of cerebral, mesenteric, coronary, and skeletal muscle microvessels [11,12,13,14,15,16].
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