This study demonstrates that NAD+ depletion in vascular endothelial cells triggers a senescence-like state that increases production of pro-inflammatory prostanoids (PGF1α and TXB2) via p38 MAPK and COX2 activation. Using FK866 to deplete NAD+, researchers showed this pathway drives vascular dysfunction associated with aging and cardiovascular disease. Crucially, NMN supplementation reversed NAD+ depletion, suppressed the senescence phenotype, and attenuated prostanoid overproduction, suggesting NAD+ restoration as a therapeutic target for age-related vascular pathology.
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NAD+ restoration via NMN suppressed senescence-related prostanoid overproduction in endothelial cells, supporting its role in vascular aging pathways.