https://doi.org/10.1...2255-019-0047-6
Nacarelli et al. took advantage of a mouse model in which expression of oncogenic KRasG12D is restricted to the pancreas. These mice develop PanINs, which progress into PDAC under stress. Remarkably, the authors demonstrated that interventions that altered the NAD+/NADH ratio affected the SASP and disease progression: treatment of mice with NMN increased precancerous and cancerous lesions, and upregulated immune-cell infiltration as well as the expression of pro-inflammatory cytokines3 . In contrast, pharmacological NAMPT inhibition with FK866 suppressed the induction of pro-inflammatory cytokines and senescence markers in the pancreas without decreasing immune infiltration or the acinar area. These findings confirm that the pro-inflammatory SASP contributes to the progression of pancreatic cancer, and this effect is aggravated by increasing NAD+ levels with NMN treatment (Fig. 1).
The blame this on NAD+ levels, but in reality the only thing they can say is the NMN did this. We don't know if NMN raising NAD had anything to do with this or not. We can only say NMN itself raised inflammation levels and increased precancerous and cancerous lesions in mice.
Edited by Michael, 11 July 2020 - 05:42 PM.