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Nicotinamide mononucleotide (NMN) supplementation
Understanding molecular mechanisms involved in vascular aging is essential to develop novel interventional strategies for treatment and prevention of agerelated vascular pathologies. Recent studies provide critical evidence that vascular aging is characterized by NAD+ depletion. Importantly, in aged mice, restoration of cellular NAD+ levels by treatment with the NAD+ booster nicotinamide mononucleotide (NMN) exerts significant vasoprotective effects, improving endotheliumdependent vasodilation, attenuating oxidative stress, and rescuing agerelated changes in gene expression. Strong experimental evidence shows that dysregulation of microRNAs (miRNAs) has a role in vascular aging. The present study was designed to test the hypothesis that agerelated NAD+ depletion is causally linked to dysregulation of vascular miRNA expression. A corollary hypothesis is that functional vascular rejuvenation in NMN-treated aged mice is also associated with restoration of a youthful vascular miRNA expression profile. To test these hypotheses, aged (24-monthold) mice were treated with NMN for 2 weeks and miRNA signatures in the aortas were compared to those in aortas obtained from untreated young and aged control mice. We found that protective effects of NMN treatment on vascular function are associated with antiaging changes in the miRNA expression profile in the aged mouse aorta. The predicted regulatory effects of NMNinduced differentially expressed miRNAs in aged vessels include antiatherogenic effects and epigenetic rejuvenation. Future studies will uncover the mechanistic role of miRNA gene expression regulatory networks in the antiaging effects of NAD+ booster treatments and determine thelinks between miRNAs regulated by NMN and sirtuin activators and miRNAs known to act in the conserved pathways of aging and major aging-related vascular diseases.