Role of nicotinamide adenine dinucleotide in cardiovascular disease.
Level 5 - mechanism / opinion, no new human data
Narrative review without systematic search methodology or original data
PubMed 42047243 · doi:10.1097/HCO.0000000000001292
What was done
This narrative review synthesizes current literature on the role of nicotinamide adenine dinucleotide (NAD+) metabolism and the rate-limiting salvage enzyme nicotinamide phosphoribosyltransferase (NAMPT) in cardiovascular pathophysiology. It reviews mechanisms involving sirtuin signaling, circadian-regulated Nampt oscillation, and therapeutic strategies utilizing NAD+ precursor supplementation.
What was found
The abstract provides no quantitative findings, statistical metrics, or patient numbers. It reports mechanistically that NAD+ content and the NAD+/NADH ratio are depleted in cardiovascular disease and heart failure, resulting in cardiomyocyte mitochondrial dysfunction, increased reactive oxygen species (ROS) production, and cell death. Therapeutic supplementation with precursors including nicotinic acid, nicotinamide, nicotinamide mononucleotide, and nicotinamide riboside is currently under clinical evaluation.
Why it matters
This review outlines the biochemical rationale for targeting NAD+ depletion and the salvage pathway as potential therapeutic interventions for heart failure and related cardiovascular disorders.
Limits
The paper is a non-systematic narrative review providing no primary clinical trial data, quantitative effect estimates, or structured methodology. Reported mechanisms rely largely on preclinical models, and clinical efficacy in human populations remains to be established in ongoing trials.
Cited by
- supports Sirtuins require NAD for fuel, and NAD requires NMN as a precursor.