NAD+

Redox Coenzyme in Bioenergetics
NAD⁺ accepts hydride ions from key metabolic pathways—glycolysis, the tricarboxylic acid (TCA) cycle, and fatty‐acid β-oxidation—to form NADH, which then donates electrons to the mitochondrial electron‐transport chain for ATP synthesis via oxidative phosphorylation
Substrate for NAD⁺-Consuming Enzymes
Serves as an obligatory co-substrate for sirtuin deacetylases (e.g., SIRT1/3), poly-ADP-ribose polymerases (PARPs), and the NADase CD38, thereby regulating protein deacetylation, DNA-damage–response ADP-ribosylation, and calcium signaling.
Modulation of Gene Expression & Stress Responses
Through SIRT1-mediated deacetylation of transcriptional regulators (e.g., PGC-1α) and PARP-driven DNA repair, NAD⁺ levels fine-tune mitochondrial biogenesis, antioxidant defenses, and genomic stability under stress conditions.
Salvage Pathway & Mitochondrial Health
The NAMPT-dependent salvage pathway recycles nicotinamide into NAD⁺, sustaining intracellular pools; conversely, age-associated CD38 upregulation degrades NAD⁺, contributing to mitochondrial dysfunction.