Fig. 9. Schematic representation of the role of cellular senescence and sterile inflammation in the regulation of CD38 and NMN degradation.
In young mice, levels of CD38+ inflammatory cells and senescent cells in tissues are lower than older mice. During aging there is an increase in senescent cells that, at least in part, through their senescence associated secretory phenotype (SASP), promotes accumulation of CD38+ immune cells. The ecto-enzymatic activity of CD38 in immune cells degrades NMN extracellularly, preventing the NMN-induced NAD+ boosting in other cells in the tissue.