NAD+ decline helps drive cardiovascular disease in mice, which can be mitigated with the precursor NMN
CD38 is the main enzyme for the degradation of nicotinamide adenine dinucleotide (NAD+) — a cofactor in 400+ critical cellular activities — a process shown to contribute to aging. In their article published in Signal Transduction and Targeted Therapy, researchers from Sichuan University and Nanchang University show that CD38 and the associated intracellular NAD+ decline are critical for processes that drive age-related cardiovascular diseases, such as atherosclerosis and hypertension.
In mice lacking CD38 or supplemented with a CD38 inhibitor or the NAD+ precursor nicotinamide mononucleotide (NMN), the researchers blocked the development of cardiovascular diseases by limiting high blood pressure and increases in blood vessel cell senescence — a permanent state when cells can no longer replicate. In addition, the researchers observed that CD38 deficiency or NAD+ supplementation remarkably mitigated senescence of blood vessel cells by suppressing signaling payloads between cells called extracellular vesicles that facilitated the senescence of neighboring non-damaged cells.