Visfatin and endothelial angiogenesis: AUTHORS' RETROSPECTIVE

Abstract

This editorial refers to an article by R. Adya et al . [2][1] published in Cardiovascular Research in 2008 (see [Box 1][2]). It is accompanied by an editorial by J. Waltenberger and E. Pardali (doi:10.1093/cvr/cvs180) as part of this Spotlight on Landmark Papers in Cardiovascular Research . We are members of the ‘Metabolic and Vascular Research Group’, Warwick Medical School, UK, interested in novel adipokines proposed to have a functional interplay with the cardiovascular system. Since the discovery of visfatin/pre-B cell colony-enhancing factor (PBEF)/NAMPT in 2004,1 researchers world-wide have contributed to our present understanding of this ever-elusive molecule. We had published previously on visfatin-mediated effects in human endothelial cells contributing to endothelial angiogenesis.2 In this short editorial, we aim to briefly recapitulate the historical perspectives and previous contributions in the field of visfatin research. PBEF (also termed nicotinamide phosphoribosyl transferase, NAMPT, or visfatin) was discovered as a novel cytokine secreted by activated human lymphocytes that functions as a growth factor for early B cell maturation.1 Despite the absence of a signal peptide required for secretion, PBEF/visfatin has been demonstrated to circulate freely in detectable ranges in plasma and serum, functioning as a classical cytokine.3,4 Pro-inflammatory properties of visfatin have been widely documented in several in vitro and in vivo studies. Earlier investigations reported both the presence of visfatin (PBEF) and its effects in inducing IL-6 and IL-8 cytokine release from amnion-like epithelial (WISH) cells and foetal membrane explants.5,6 Later studies elucidated the role of visfatin in delaying neutrophil apoptosis in experimental inflammation/clinical sepsis7 and thrombin-induced … [1]: #ref-2 [2]: #F3