Mechanism of Action
NAD⁺ is an essential pyridine dinucleotide coenzyme functioning as a central electron carrier in cellular metabolism. As a hydride acceptor, NAD⁺ is reduced to NADH during glycolysis, the TCA cycle, and β-oxidation of fatty acids, with NADH subsequently donating electrons to the mitochondrial electron transport chain (Complex I) to drive ATP synthesis via oxidative phosphorylation.
Beyond metabolism, NAD⁺ serves as the obligate substrate for three regulatory enzyme families: Sirtuins (SIRT1–SIRT7) — NAD⁺-dependent deacylases regulating gene expression, DNA repair, and mitochondrial biogenesis via PGC-1α; PARPs — NAD⁺-consuming enzymes central to DNA strand-break detection and repair; and CD38/CD157 — NAD⁺ glycohydrolases generating cyclic ADP-ribose for Ca²⁺ signaling.
Intracellular NAD⁺ levels decline with age across multiple tissues, linked to reduced mitochondrial function, impaired DNA repair capacity, and altered sirtuin activity. This NAD⁺ depletion hypothesis has driven substantial preclinical interest in NAD⁺ biosynthesis pathway research.
