This 2018 paper argues that nicotinamide increase SIRT1 activity in cells and activates autophagy and mitophagy. Reference 18. in this paper is the same as has been discussed in this thread.
Nicotinamide (NAM), an amide form of vitamin B3, is a potent inhibitor of sirtuins, a family of NAD+-dependent deacetylases. The sirtuin family proteins, of which SIRT1 is the best known, play critical roles in cellular and organismal health and longevity (17), and NAM has been predicted to negatively affect cell viability. However, in cells NAM is rapidly converted to NAD+ through a salvage pathway, and therefore treatment with NAM has been found to increase SIRT1 activity (18). As a result, NAM appears to protect cells against oxidative stress in a number of studies, including ours. For example, administration of 5 mM NAM caused a decrease in mitochondrial superoxide levels and resulted in substantial extension of proliferative potential in normal fibroblasts (19). The treated cells showed a decrease in mitochondria content but an increase in their quality as evidenced by lower levels of ROS generation and oxidative damage to mitochondrial proteins. These changes might be due at least in part to activation of autophagy (and mitophagy) through SIRT1 mobilization driven by the NAM-induced increases in the NAD+/NADH ratio (20).
http://www.ijstemcel...ge=13&year=2018
18. Hwang, ES, and Song, SB (2017). Nicotinamide is an inhibitor of SIRT1 in vitro, but can be a stimulator in cells. Cell Mol Life Sci. 74, 3347-3362.
19. Kang, HT, Lee, HI, and Hwang, ES (2006). Nicotinamide extends replicative lifespan of human cells. Aging Cell. 5, 423-436.
20. Jang, SY, Kang, HT, and Hwang, ES (2012). Nicotinamide-induced mitophagy: event mediated by high NAD+/NADH ratio and SIRT1 protein activation. J Biol Chem. 287, 19304-19314.