Nicotinamide Mononucleotide Improves Blood Vessel Function by Converting to Nicotinamide Riboside: Preclinical Findings

Synopsis

Nicotinamide mononucleotide (NMN) and nicotinamide riboside (NR) are compounds that help make NAD+, which may protect blood vessels. Researchers studied how NMN and NR affect inflammation and dysfunction in endothelial cells, which line blood vessels, and whether an enzyme called CD73 plays a role. In human endothelial cells, NMN and NR reduced inflammation caused by IL1β or TNFα, shown by lower levels of inflammatory markers ICAM1 and vWF. When CD73 was blocked, the anti-inflammatory effect of NMN was lost, but NR’s effect stayed the same. Interestingly, inflammation increased NAD levels inside the cells, along with enzymes NAMPT and CD73, while CD38 changed less. NMN and NR further raised NAD levels in inflamed cells, but blocking CD73 stopped the NAD increase caused by NMN—not the increase caused by NR. In mouse aortic rings, angiotensin II impaired blood vessel relaxation, but both NMN and NR prevented this dysfunction. In aortic rings from mice without CD73, NMN no longer worked, but NR still did. This shows that NMN and NR improve blood vessel function and reduce inflammation by raising intracellular NAD through both CD73-dependent (for NMN) and CD73-independent (for NR) mechanisms. The conversion of NMN to NR by CD73 on endothelial surfaces is an important way to protect blood vessels and maintain NAD inside cells.

Journal

Biochemical Pharmacology