Micronutrients & recovery
Overexpression of Nicotinamide Phosphoribosyltransferase (Nampt) extends the replicative lifespan of human vascular smooth muscle cells and fibroblasts by activating SIRT1 and promoting p53 degradation.
This research identifies Nampt (an enzyme that recycles NAD+) as a critical regulator of cellular aging in vascular cells. While this paper uses genetic overexpression in a lab setting, it suggests that maintaining or boosting NAD+ salvage pathways (potentially through precursors like Nicotinamide Riboside or Nicotinamide Mononucleotide) might support vascular health and delay cellular senescence. Current evidence is preclinical, so this is a mechanistic insight rather than a direct prescription.
introducing the Nampt gene into aging human SMCs delayed senescence and substantially lengthened cell lifespan... Nampt-mediated SMC lifespan extension was associated with increased activity of the NAD(+)-dependent longevity enzyme SIRT1... These data indicate that Nampt is a longevity protein that can add stress-resistant life to human SMCs by optimizing SIRT1-mediated p53 degradation.
Why this rating
The study is an in vitro cell culture study using human vascular smooth muscle cells and fibroblasts; it does not involve human clinical trials or in vivo animal models.
Source
Extension of Human Cell Lifespan by Nicotinamide Phosphoribosyltransferase
Eric van der Veer et al. · Journal of Biological Chemistry · 2007
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