Study summary · research use only
NAD(+) metabolism: pathophysiologic mechanisms and therapeutic potential
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This review discusses NAD+ and its metabolites as regulators of physiological processes that allow cells to adapt to environmental changes such as nutrient perturbation, genotoxic factors, circadian disruption, infection, inflammation, and xenobiotics. The authors describe NAD+'s role as an enzyme cofactor in oxidation-reduction reactions, chemical modification of DNA, RNA, and proteins by NAD+-dependent enzymes, and release of the second messengers cyclic ADP-ribose and NAADP+. The abstract states that prolonged disequilibrium of NAD+ metabolism is associated with disturbed physiological function and diseases including metabolic disease, cancer, aging, and neurodegenerative disorders, and it discusses potential avenues for therapeutic intervention. Species and study type are not specified.
Abstract
Nicotinamide adenine dinucleotide (NAD+) and its metabolites function as critical regulators to maintain physiologic processes, enabling the plastic cells to adapt to environmental changes including nutrient perturbation, genotoxic factors, circadian disorder, infection, inflammation and xenobiotics. These effects are mainly achieved by the driving effect of NAD+ on metabolic pathways as enzyme cofactors transferring hydrogen in oxidation-reduction reactions. Besides, multiple NAD+-dependent enzymes are involved in physiology either by post-synthesis chemical modification of DNA, RNA and proteins, or releasing second messenger cyclic ADP-ribose (cADPR) and NAADP+. Prolonged disequilibrium of NAD+ metabolism disturbs the physiological functions, resulting in diseases including metabolic diseases, cancer, aging and neurodegeneration disorder. In this review, we summarize recent advances in our understanding of the molecular mechanisms of NAD+-regulated physiological responses to stresses, the contribution of NAD+ deficiency to various diseases via manipulating cellular communication networks and the potential new avenues for therapeutic intervention.
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