Nicotinamide adenine dinucleotide (NAD+), an important metabolite and signaling molecule in all human cells. Emerging evidence strongly suggests that NAD+ is a key player in aging, neurodegeneration and metabolic diseases.
NAD+ loss has direct and indirect consequences on multiple cellular endpoints. Ultimately, depletion of intracellular NAD+ alters the NAD+/SIRT1 axis and leads to defects in mitochondrial homeostasis, ROS production, DNA repair and cell survival.
The maintenance of the mitochondrial NAD+ pool is also of crucial importance. The biosynthesis, transport, and catabolism of NAD+ and its key intermediates play an important role in the regulation of NAD-consuming mediators.
Nicotinamide adenine dinucleotide (NAD+) is essential for maintaining cellular redox homeostasis and for modulating numerous biological events, including cellular metabolism.
The tight connection between NAD+ and sirtuins is regulated at several different levels, adding further complexity to their coordination in metabolic and aging/longevity control. Interestingly, it has been demonstrated that NAD+ availability decreases with age, reducing sirtuin activity and affecting the communication between the nucleus and mitochondria at a cellular level and also between the hypothalamus and adipose tissue at a systemic level.
