Invited Review ArticleNAMPT and NAMPT-controlled NAD Metabolism in Vascular RepairWang, Pei MD, PhD; Li, Wen-Lin PhD; Liu, Jian-Min MD; Miao, Chao-Yu MD, PhDAuthor Information Departments of *Pharmacology; and †Cell Biology, Second Military Medical University, Shanghai, China; ‡Department of Neurosurgery, Stroke Center, Changhai Hospital, Second Military Medical University, Shanghai, China; and §Center of Stroke, Beijing Institute for Brain Disorders, Beijing, China. Reprints: Chao-Yu Miao, MD, PhD or Pei Wang, MD, PhD, Department of Pharmacology, Second Military Medical University, Shanghai, China 200433 (e-mail: firstname.lastname@example.org; email@example.com). Supported by grants from the National Natural Science Foundation of China (81373414, 81130061, 81422049, and 81473208), the National 863 Plan Young Scientist Program (2015AA020943), and Shanghai Qimingxing Program (14QA1404700). The authors report no conflicts of interest. Received August 25, 2015 Accepted September 30, 2015 Journal of Cardiovascular Pharmacology: June 2016 - Volume 67 - Issue 6 - p 474-481 doi: 10.1097/FJC.0000000000000332 Buy Metrics Abstract 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. Copyright © 2016 Wolters Kluwer Health, Inc. All rights reserved.