Fig. 3. Signal pathway of the anti-aging effect of nicotinamide mononucleotide (NMN). NMN facilitates the synthesis of nicotinamide adenine dinucleotide (NAD⁺), resulting in reduced levels of NAD⁺-consuming enzymes, such as cluster of differentiation 38 (CD38) and poly(adenosine diphosphate (ADP)-ribose) polymerase-1 (PARP-1), thereby modulating immune function and reprogramming macrophage phenotypes towards increased activation of the anti-inflammatory M2 phenotype. As the primary consumers of NAD⁺, the activation of sirtuins due to elevated levels of NAD⁺ orchestrates the regulation of critical metabolic processes, stress responses, and the biology of aging via the activation or inhibition of downstream signaling pathways, ultimately exerting an anti-aging effect. AMPK: adenosine 5'-monophosphate (AMP)-activated protein kinase; FOXO: forkhead box protein O; IL: interleukin; mTOR: mammalian target of rapamycin; NAM: nicotinamide; NF-κB: nuclear factor-κB;TGF-β: transforming growth factor-β; TNFα: tumor necrosis factor α;SOD2: superoxide dismutase 2; UPR^mt: mitochondrial unfolded protein response.