NAMPT and NAMPT-controlled NAD Metabolism in Vascular Repair

• Published in: Journal of cardiovascular pharmacology Vol. 67; no. 6; p. 474
• Main Authors: Wang, Pei, Li, Wen-Lin, Liu, Jian-Min, Miao, Chao-Yu
• Format: Journal Article
• Language: English
• Published: United States 01.06.2016
• Subjects: ADP-ribosyl Cyclase 1 - metabolism; Endothelial Cells - metabolism; Endothelial Progenitor Cells - metabolism; Muscle, Smooth, Vascular - metabolism; NAD - metabolism; Nicotinamide Phosphoribosyltransferase - metabolism; Poly(ADP-ribose) Polymerases - metabolism; Signal Transduction; Sirtuins - metabolism
• ISSN: 1533-4023
• DOI: 10.1097/FJC.0000000000000332

Vascular repair plays important roles in postischemic remodeling and rehabilitation in cardiovascular and cerebrovascular disease, such as stroke and myocardial infarction. Nicotinamide adenine dinucleotide (NAD), a well-known coenzyme involved in electron transport chain for generation of adenosine triphosphate, has emerged as an important controller regulating various biological signaling pathways. Nicotinamide phosphoribosyltransferase (NAMPT) is the rate-limiting enzyme for NAD biosynthesis in mammals. NAMPT may also act in a nonenzymatic manner, presumably mediated by unknown receptor(s). Rapidly accumulating data in the past decade show that NAMPT and NAMPT-controlled NAD metabolism regulate fundamental biological functions in endothelial cells, vascular smooth muscle cells, and endothelial progenitor cells. The NAD-consuming proteins, including sirtuins, poly-ADP-ribose polymerases (PARPs), and CD38, may contribute to the regulatory effects of NAMPT-NAD axis in these cells and vascular repair. This review discusses the current data regarding NAMPT and NAMPT-controlled NAD metabolism in vascular repair and the clinical potential translational application of NAMPT-related products in treatment of cardiovascular and cerebrovascular disease.