NAMPT was identified as being substantially upregulated as SMCs entered a program of differentiation and enhanced resistance to stress. When first discovered, Nampt was thought to be a cytokine and was termed pre-B-cell colony-enhancing factor (PBEF). However, the present authors and two other groups subsequently revealed its role instead as an enzyme in the NAD+ salvage pathway.There are also several reports, and many review articles, discussing Nampt as an adipokine termed visfatin.
However, the index report in Science describing an adipokine role for Nampt has now been retracted. In addition, the often contradictory findings relating circulating Nampt (visfatin) to various metabolic conditions are confounded by the uncertain validity of Nampt enzyme-linked immunosorbent assay (ELISA) kits that rapidly appeared on the market after the initial report in Science. There is evidence, however, that an extracellular form of Nampt might have important actions, including regulating glucose uptake in tissues that do not synthesize significant amounts of Nampt, such as the brain. The extent to which the release of Nampt from cells is regulated is uncertain. Regardless, locally produced Nampt is likely to be important to several organs and Nampt has been found to be expressed in endothelial cells, SMCs and kidney-derived mesangial cells.
