Cd38, a transmembrane glycoprotein, can act as an enzyme with NAD-depleting and intracellular signaling activity, or as a receptor with adhesive functions [2]. It is widely expressed in hematopoietic cells, multiple myeloma (MM) cells, and some non-hematopoietic tissues [3,5]. Cd38 is involved in regulating intracellular nicotinamide adenine dinucleotide (NAD+) levels, which is crucial for various cellular functions and signaling pathways [1,2,6,7].

Cd38 knockout (KO) mouse models have shown significant protective effects against neurodegenerative and neuroinflammatory insults [1]. In the context of ovarian aging, CD38 deletion mitigated ovarian aging, preserving fertility and follicle reserve in aged mice by countering age-related gene expression changes and intercellular communication alterations [4]. Also, inflammation-induced increase in CD38 in immune cells during aging leads to decreased NAD+ levels, and blocking its ecto-enzymatic activity can increase NAD+ [6].

In conclusion, Cd38 plays essential roles in multiple biological processes including neurodegeneration, neuroinflammation, ovarian aging, and immune cell function through its regulation of NAD+ levels. The use of Cd38 KO mouse models has provided valuable insights into its functions in these disease-related areas, highlighting its potential as a therapeutic target [1,4,6].