Nicotinamide adenine dinucleotide (NAD
+) is pivotal to physiological processes, not only as the coenzyme of cellular oxidation–reduction reactions but also for the activation of NAD
+-consuming enzymes, such as sirtuins, poly-ADP-ribose polymerases (PARPs), cADP-ribose synthases, NADase (CD38), and mono-ADP-ribose transferases (ARTs) [1]. NAD
+ participates in more than 50% of all physiological processes, including mitochondrial biogenesis, cardiovascular protection, neuroprotection, oxidative stress, DNA damage repair, stem cell rejuvenation, and inflammation [2]. Low NAD
+ levels are associated with age-associated physical disability and diseases, such as metabolic syndrome and cardiovascular disease [1,2,3]. The NAD
+ salvage pathway, which utilizes NAD
+ precursors, is the predominant mechanism for maintaining cellular NAD