Nitric oxide and angiogenesis in cardiovascular disease.

Ischemic heart disease and peripheral artery disease mainly develop as a consequence of atherosclerotic lesion formation. Angiogenesis, the formation of new blood vessels from the preexisting vascular bed, is of paramount importance in the maintenance of vascular integrity both in the repair process of damaged tissue (wound healing) and in the formation of collateral vessels in response to tissue ischemia. Angiogenesis is a complex process that is orchestrated by a multitude of cytokines/chemokines and growth factors. In its broadest sense, angiogenesis cannot be viewed as a single process. It is likely that different mediators are involved in different phases of angiogenesis. Vascular endothelial cells produce nitric oxide (NO), an endothelium-derived labile molecule, which maintains vascular homeostasis and thereby prevents vascular atherosclerotic changes. In patients with ischemic heart disease and peripheral artery disease, the release of endothelium-derived NO is decreased, which plays an important role in the atherosclerotic disease progression. In recent years, endothelium-derived NO has been shown to modulate angiogenesis in vitro and in vivo. In this review, we summarize recent progress in the field of the NO-mediated regulation of postnatal angiogenesis.