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Nutrients
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Nicotinamide Adenine Dinucleotide (NAD) in Human Health and Disease
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Nicotinamide Adenine Dinucleotide (NAD) in Human Health and Disease

A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Nutrition and Metabolism".

Deadline for manuscript submissions: closed (30 September 2021) | Viewed by 19489

Special Issue Editor

Dr. Fiammetta Monacelli

E-Mail Website
Guest Editor
Department of Internal Medicine and Medical Specialties (DIMI), Section of Geriatrics, University of Genoa, 16132 Genoa, Italy
Interests: geriatrics; frail elderly; dementia; oncogeriatrics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Nicotinamide adenine dinucleotide (NAD+) is both a coenzyme for hydride-transfer enzymes and a substrate for NAD+-consuming enzymes, which include ADP-ribose transferases, poly(ADP-ribose) polymerases, cADP-ribose synthases, and sirtuins. As result, it represents the heart of metabolic activity in all living cells. Recent results establish protective roles for NAD+ that might be therapeutically applicable for the prevention of neurodegenerative conditions and to fight cancers. Importantly, the NAD+ biosynthetic apparatus emerges as a collection of potential therapeutic targets, for some of which (e.g., nicotinamide phosphoribosyltransferase (NAMPT)) a role in carcinogenesis and aging is already largely established.

This Special Issue will focus on the current understanding of NAD’s role in human health and disease to fully provide in-depth insights into the correlation between energy metabolism and human health, as well as its effects on the pathogenesis of age-related decline and disease.

We invite authors to contribute original research articles as well as review articles. Potential topics include, but are not limited to:

  • NAD-metabolism targeting in aging and age-related diseases.
  • Novel therapeutic vulnerabilities in the NAD biosynthetic apparatus, including epigenetics.
  • Metabolic dysfunctions in human health and disease.
  • NAD+-boosting strategies and anti-tumor immunotherapies.

Dr. Fiammetta Monacelli
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Nutrients is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • human health
  • metabolism
  • aging
  • cancer
  • immunotherapies

Published Papers (3 papers)

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Review

16 pages, 865 KiB  
Review
Age-Dependent Decline of NAD+—Universal Truth or Confounded Consensus?
by Augusto Peluso, Mads V. Damgaard, Marcelo A. S. Mori and Jonas T. Treebak
Nutrients 2022, 14(1), 101; https://0-doi-org.brum.beds.ac.uk/10.3390/nu14010101 - 27 Dec 2021
Cited by 18 | Viewed by 6741
Abstract
Nicotinamide adenine dinucleotide (NAD+) is an essential molecule involved in various metabolic reactions, acting as an electron donor in the electron transport chain and as a co-factor for NAD+-dependent enzymes. In the early 2000s, reports that NAD+ declines [...] Read more.
Nicotinamide adenine dinucleotide (NAD+) is an essential molecule involved in various metabolic reactions, acting as an electron donor in the electron transport chain and as a co-factor for NAD+-dependent enzymes. In the early 2000s, reports that NAD+ declines with aging introduced the notion that NAD+ metabolism is globally and progressively impaired with age. Since then, NAD+ became an attractive target for potential pharmacological therapies aiming to increase NAD+ levels to promote vitality and protect against age-related diseases. This review summarizes and discusses a collection of studies that report the levels of NAD+ with aging in different species (i.e., yeast, C. elegans, rat, mouse, monkey, and human), to determine whether the notion that overall NAD+ levels decrease with aging stands true. We find that, despite systematic claims of overall changes in NAD+ levels with aging, the evidence to support such claims is very limited and often restricted to a single tissue or cell type. This is particularly true in humans, where the development of NAD+ levels during aging is still poorly characterized. There is a need for much larger, preferably longitudinal, studies to assess how NAD+ levels develop with aging in various tissues. This will strengthen our conclusions on NAD metabolism during aging and should provide a foundation for better pharmacological targeting of relevant tissues. Full article
(This article belongs to the Special Issue Nicotinamide Adenine Dinucleotide (NAD) in Human Health and Disease)
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11 pages, 862 KiB  
Review
Role of CD38 in Adipose Tissue: Tuning Coenzyme Availability?
by Andrea Benzi, Alessia Grozio, Sonia Spinelli, Laura Sturla, Andreas H. Guse, Antonio De Flora, Elena Zocchi, Joerg Heeren and Santina Bruzzone
Nutrients 2021, 13(11), 3734; https://0-doi-org.brum.beds.ac.uk/10.3390/nu13113734 - 23 Oct 2021
Cited by 3 | Viewed by 2601
Abstract
Nicotinamide adenine dinucleotide (NAD+) is a fundamental molecule in the regulation of energy metabolism, representing both a coenzyme and a substrate for different NAD+ degrading enzymes. Among these enzymes, CD38 can be seen under two perspectives: as the enzyme synthesizing [...] Read more.
Nicotinamide adenine dinucleotide (NAD+) is a fundamental molecule in the regulation of energy metabolism, representing both a coenzyme and a substrate for different NAD+ degrading enzymes. Among these enzymes, CD38 can be seen under two perspectives: as the enzyme synthesizing Ca2+-mobilizing second messenger, starting from NAD+, and as the major NAD+-consumer, to be inhibited to increase NAD+ levels. Indeed, the regulation of NAD+ availability is a key event during different processes. In this review, we examine the recent studies related to the modulation of CD38 expression and activity, and the consequent changes in NAD(P)(H), in adipose tissue, during inflammation and cold-induced thermogenesis. Full article
(This article belongs to the Special Issue Nicotinamide Adenine Dinucleotide (NAD) in Human Health and Disease)
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35 pages, 1203 KiB  
Review
Advances in NAD-Lowering Agents for Cancer Treatment
by Moustafa S. Ghanem, Fiammetta Monacelli and Alessio Nencioni
Nutrients 2021, 13(5), 1665; https://0-doi-org.brum.beds.ac.uk/10.3390/nu13051665 - 14 May 2021
Cited by 39 | Viewed by 9072
Abstract
Nicotinamide adenine dinucleotide (NAD) is an essential redox cofactor, but it also acts as a substrate for NAD-consuming enzymes, regulating cellular events such as DNA repair and gene expression. Since such processes are fundamental to support cancer cell survival and proliferation, sustained NAD [...] Read more.
Nicotinamide adenine dinucleotide (NAD) is an essential redox cofactor, but it also acts as a substrate for NAD-consuming enzymes, regulating cellular events such as DNA repair and gene expression. Since such processes are fundamental to support cancer cell survival and proliferation, sustained NAD production is a hallmark of many types of neoplasms. Depleting intratumor NAD levels, mainly through interference with the NAD-biosynthetic machinery, has emerged as a promising anti-cancer strategy. NAD can be generated from tryptophan or nicotinic acid. In addition, the “salvage pathway” of NAD production, which uses nicotinamide, a byproduct of NAD degradation, as a substrate, is also widely active in mammalian cells and appears to be highly exploited by a subset of human cancers. In fact, research has mainly focused on inhibiting the key enzyme of the latter NAD production route, nicotinamide phosphoribosyltransferase (NAMPT), leading to the identification of numerous inhibitors, including FK866 and CHS-828. Unfortunately, the clinical activity of these agents proved limited, suggesting that the approaches for targeting NAD production in tumors need to be refined. In this contribution, we highlight the recent advancements in this field, including an overview of the NAD-lowering compounds that have been reported so far and the related in vitro and in vivo studies. We also describe the key NAD-producing pathways and their regulation in cancer cells. Finally, we summarize the approaches that have been explored to optimize the therapeutic response to NAMPT inhibitors in cancer. Full article
(This article belongs to the Special Issue Nicotinamide Adenine Dinucleotide (NAD) in Human Health and Disease)
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