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NAD(+) homeostasis in human health and disease
Depletion of nicotinamide adenine dinucleotide (NAD(+)), a central redox cofactor and the substrate of key metabolic enzymes, is the causative factor of a number of inherited and acquired diseases in humans. Primary deficiencies of NAD(+) homeostasis are the result of impaired biosynthesis, while se...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8261484/ https://www.ncbi.nlm.nih.gov/pubmed/34041853 http://dx.doi.org/10.15252/emmm.202113943 |
Sumario: | Depletion of nicotinamide adenine dinucleotide (NAD(+)), a central redox cofactor and the substrate of key metabolic enzymes, is the causative factor of a number of inherited and acquired diseases in humans. Primary deficiencies of NAD(+) homeostasis are the result of impaired biosynthesis, while secondary deficiencies can arise due to other factors affecting NAD(+) homeostasis, such as increased NAD(+) consumption or dietary deficiency of its vitamin B3 precursors. NAD(+) depletion can manifest in a wide variety of pathological phenotypes, ranging from rare inherited defects, characterized by congenital malformations, retinal degeneration, and/or encephalopathy, to more common multifactorial, often age‐related, diseases. Here, we discuss NAD(+) biochemistry and metabolism and provide an overview of the etiology and pathological consequences of alterations of the NAD(+) metabolism in humans. Finally, we discuss the state of the art of the potential therapeutic implications of NAD(+) repletion for boosting health as well as treating rare and common diseases, and the possibilities to achieve this by means of the different NAD(+)‐enhancing agents. |
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