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Biomolecules
Special Issues
NAD Metabolism in Physiology and Pathology
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NAD Metabolism in Physiology and Pathology

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: closed (30 October 2024) | Viewed by 5438

Special Issue Editor

Prof. Dr. Mathias Ziegler

E-Mail Website
Guest Editor
Department of Biomedicine, University of Bergen, Bergen, Norway
Interests: NAD; metabolic signaling; enzymology

Special Issue Information

Dear Colleagues,

Nicotinamide adenine dinucleotide (NAD) and its metabolites function as critical regulators to maintain cellular processes. Serving as a crucial co-enzyme for redox reactions and substrate for NAD-dependent enzymes, NAD and its metabolites act as a regulatory hub controlling a broad range of physiological processes, including redox homeostasis, genomic stability, gene expression, RNA processing, energy metabolism, immunity and inflammation, and the circadian clock. Given the essential roles of NAD in most biological processes, NAD metabolic abnormalities represent major contributors to the pathophysiology of various diseases, such as infections, cancers, metabolic diseases, aging, and age-associated neurodegenerative disorders.

This Special Issue aims to provide novel insights into NAD metabolism in physiology and pathology. We welcome original research and review articles on these topics.

Prof. Dr. Mathias Ziegler
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. Biomolecules is an international peer-reviewed open access monthly 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 2700 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

  • NAD
  • ADP-ribosylation
  • sirtuins
  • redox homeostasis
  • NAD glycohydrolases

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Published Papers (3 papers)

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Research

16 pages, 1148 KiB  
Article
NADH Reductive Stress and Its Correlation with Disease Severity in Leigh Syndrome: A Pilot Study Using Patient Fibroblasts and a Mouse Model
by Tamaki Ishima, Natsuka Kimura, Mizuki Kobayashi, Chika Watanabe, Eriko F. Jimbo, Ryosuke Kobayashi, Takuro Horii, Izuho Hatada, Kei Murayama, Akira Ohtake, Ryozo Nagai, Hitoshi Osaka and Kenichi Aizawa
Biomolecules 2025, 15(1), 38; https://doi.org/10.3390/biom15010038 - 31 Dec 2024
Viewed by 1361
Abstract
Nicotinamide adenine dinucleotide (NAD) is a critical cofactor in mitochondrial energy production. The NADH/NAD+ ratio, reflecting the balance between NADH (reduced) and NAD+ (oxidized), is a key marker for the severity of mitochondrial diseases. We recently developed a [...] Read more.
Nicotinamide adenine dinucleotide (NAD) is a critical cofactor in mitochondrial energy production. The NADH/NAD+ ratio, reflecting the balance between NADH (reduced) and NAD+ (oxidized), is a key marker for the severity of mitochondrial diseases. We recently developed a streamlined LC-MS/MS method for the precise measurement of NADH and NAD+. Utilizing this technique, we quantified NADH and NAD+ levels in fibroblasts derived from pediatric patients and in a Leigh syndrome mouse model in which mitochondrial respiratory chain complex I subunit Ndufs4 is knocked out (KO). In patient-derived fibroblasts, NAD+ levels did not differ significantly from those of healthy controls (p = 0.79); however, NADH levels were significantly elevated (p = 0.04), indicating increased NADH reductive stress. This increase, observed despite comparable total NAD(H) levels between the groups, was attributed to elevated NADH levels. Similarly, in the mouse model, NADH levels were significantly increased in the KO group (p = 0.002), further suggesting that NADH elevation drives reductive stress. This precise method for NADH measurement is expected to outperform conventional assays, such as those for lactate, providing a simpler and more reliable means of assessing disease progression. Full article
(This article belongs to the Special Issue NAD Metabolism in Physiology and Pathology)
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11 pages, 920 KiB  
Article
Role of Nicotinamide in the Pathogenesis of Actinic Keratosis: Implications for NAD+/SIRT1 Pathway
by Riccardo Belardi, Francesca Pacifici, Terenzio Cosio, Sara Lambiase, Ruslana Gaeta Shumak, Fabio Artosi, Antonia Rivieccio, Danilo Cavalloro, Elena Dellambra, Luca Bianchi, David Della-Morte and Elena Campione
Biomolecules 2024, 14(12), 1512; https://doi.org/10.3390/biom14121512 - 27 Nov 2024
Viewed by 1447
Abstract
Actinic keratosis (AK) is a precursor to invasive squamous cell carcinoma, making early diagnosis and treatment essential to prevent progression. Among available therapeutic options, nicotinamide (NAM) has shown potential in reducing AK progression. NAM is a precursor of nicotinamide adenine dinucleotide (NAD+ [...] Read more.
Actinic keratosis (AK) is a precursor to invasive squamous cell carcinoma, making early diagnosis and treatment essential to prevent progression. Among available therapeutic options, nicotinamide (NAM) has shown potential in reducing AK progression. NAM is a precursor of nicotinamide adenine dinucleotide (NAD+), which activates sirtuin (SIRT)1, a protein with anti-cancer properties. Although the role of SIRT1 in AK is still debated, no data currently exist on the systemic modulation of this protein in AK. Therefore, this study aims to evaluate whether NAM, by increasing serum NAD+ levels, may promote SIRT1 activation in peripheral blood mononuclear cells (PBMCs) in AK patients. Thirty patients were enrolled and treated with NAM for 24 months. Hematological, biochemical, and skin condition assessments were conducted, alongside the measurement of SIRT1 and NAD+ levels. A decrease in basophils, monocytes, total cholesterol, and blood glucose levels was observed in the study group, along with a reduction in AK lesions. Notably, NAM treatment significantly enhanced serum NAD+ levels, and nuclear SIRT1 activity in PBMCs. In conclusion, NAM administration significantly reduced AK progression in a NAD+/SIRT1-dependent manner, supporting its role as a chemopreventive agent in AK management. Full article
(This article belongs to the Special Issue NAD Metabolism in Physiology and Pathology)
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11 pages, 1327 KiB  
Article
Accounting for NAD Concentrations in Genome-Scale Metabolic Models Captures Important Metabolic Alterations in NAD-Depleted Systems
by Roland Sauter, Suraj Sharma and Ines Heiland
Biomolecules 2024, 14(5), 602; https://doi.org/10.3390/biom14050602 - 20 May 2024
Cited by 2 | Viewed by 1859
Abstract
Nicotinamide adenine dinucleotide (NAD) is a ubiquitous molecule found within all cells, acting as a crucial coenzyme in numerous metabolic reactions. It plays a vital role in energy metabolism, cellular signaling, and DNA repair. Notably, NAD levels decline naturally with age, and this [...] Read more.
Nicotinamide adenine dinucleotide (NAD) is a ubiquitous molecule found within all cells, acting as a crucial coenzyme in numerous metabolic reactions. It plays a vital role in energy metabolism, cellular signaling, and DNA repair. Notably, NAD levels decline naturally with age, and this decline is associated with the development of various age-related diseases. Despite this established link, current genome-scale metabolic models, which offer powerful tools for understanding cellular metabolism, do not account for the dynamic changes in NAD concentration. This impedes our understanding of a fluctuating NAD level’s impact on cellular metabolism and its contribution to age-related pathologies. To bridge this gap in our knowledge, we have devised a novel method that integrates altered NAD concentration into genome-scale models of human metabolism. This approach allows us to accurately reflect the changes in fatty acid metabolism, glycolysis, and oxidative phosphorylation observed experimentally in an engineered human cell line with a compromised level of subcellular NAD. Full article
(This article belongs to the Special Issue NAD Metabolism in Physiology and Pathology)
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