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Mediators of Inflammation
Volume 2013 (2013), Article ID 946427, 15 pages
Review Article

Visfatin/Nampt: An Adipokine with Cardiovascular Impact

1Paul-Langerhans Group of Integrative Physiology, German Diabetes Center, Auf'm Hennekamp 65, 40225 Düsseldorf, Germany
2Departamento de Farmacología y Terapéutica, Facultad de Medicina, Universidad Autónoma de Madrid, Arzobispo Morcillo 4, 28029 Madrid, Spain

Received 1 April 2013; Accepted 20 May 2013

Academic Editor: Assaf Rudich

Copyright © 2013 Tania Romacho et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Adipose tissue is acknowledged as an endocrine organ that releases bioactive factors termed adipokines. Visfatin was initially identified as a novel adipokine with insulin-mimetic properties in mice. This adipokine was identical to two previously described molecules, namely, pre-B cell colony-enhancing factor (PBEF) and the enzyme nicotinamide phosphoribosyltransferase (Nampt). Enhanced circulating visfatin/Nampt levels have been reported in metabolic diseases, such as obesity and type 2 diabetes. Moreover, visfatin/Nampt circulating levels correlate with markers of systemic inflammation. In cardiovascular diseases, visfatin/Nampt was initially proposed as a clinical marker of atherosclerosis, endothelial dysfunction, and vascular damage, with a potential prognostic value. Nevertheless, beyond being a surrogate clinical marker, visfatin/Nampt is an active player promoting vascular inflammation, and atherosclerosis. Visfatin/Nampt effects on cytokine and chemokine secretion, macrophage survival, leukocyte recruitment by endothelial cells, vascular smooth muscle inflammation and plaque destabilization make of this adipokine an active factor in the development and progression of atherosclerosis. Further research is required to fully understand the mechanisms mediating the cellular actions of this adipokine and to better characterize the factors regulating visfatin/Nampt expression and release in all these pathologic scenarios. Only then, we will be able to conclude whether visfatin/Nampt is a therapeutical target in cardiometabolic diseases.