Impairment of an Endothelial NAD + -H 2 S Signaling Network Is a Reversible Cause of Vascular Aging.
Level 5 - mechanism / opinion, no new human data
Preclinical animal and laboratory study
PubMed 29570999 · doi:10.1016/j.cell.2018.02.008
What was done
Investigated the role of endothelial SIRT1 and an NAD+-H2S signaling network in age-related vascular decline. Aged mice were treated with the NAD+ precursor nicotinamide mononucleotide (NMN), alone or combined with exercise or hydrogen sulfide (H2S), to assess changes in capillary density, blood flow, and endurance.
What was found
The abstract reports no numerical figures or confidence intervals. NMN treatment in aged mice promoted SIRT1-dependent increases in capillary density, improved blood flow, and enhanced exercise endurance. These effects were further augmented by exercise or elevation of H2S levels.
Why it matters
Provides a mechanistic framework linking endothelial NAD+ signaling and microvascular rarefaction in aging, highlighting a preclinical rationale for NAD+ boosters and exercise to restore tissue perfusion.
Limits
Findings are entirely derived from mouse models, and direct translation to human vascular aging remains unproven. The abstract omits sample sizes, specific NMN dosages, treatment durations, and quantitative effect sizes.
Cited by
- supports Sinclair's lab published a paper in 2012 demonstrating that diminished blood flow is a pernicious driver of aging and can be reversed with NMN via SIRT1.