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Metabolites
Special Issues
Reactive Oxygen Species and Metabolic Dysregulation: From Bench to Bedside
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Reactive Oxygen Species and Metabolic Dysregulation: From Bench to Bedside

A special issue of Metabolites (ISSN 2218-1989). This special issue belongs to the section "Cell Metabolism".

Deadline for manuscript submissions: 15 March 2027 | Viewed by 312

Editors

Dr. Paola Maycotte

E-Mail Website
Guest Editor
Centro de Investigación Biomédica de Oriente, Instituto Mexicano del Seguro Social, Puebla 74360, Mexico
Interests: mitochondria; autophagy; cellular metabolism; cancer; breast cancer; cervical cancer
Special Issues, Collections and Topics in MDPI journals
Dr. Álvaro Marín-Hernández

E-Mail Website1 Website2
Guest Editor
Departamento de Bioquímica, Instituto Nacional de Cardiología, Mexico City 14080, Mexico
Interests: mitochondria; intermediary metabolism; glycolysis; cancer; enzyme
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Annie Joubert

E-Mail Website
Guest Editor
School of Medicine, Faculty of Health Sciences, University of Pretoria, Pretoria 0031, South Africa
Interests: apoptosis; cell signaling; autophagy; cancer cell biology; reactive oxygen species

Special Issue Information

Dear Colleagues,

Cellular alterations in energy metabolism and metabolic reprogramming are considered hallmarks of diverse diseases including cancer, neurodegenerative diseases, and metabolic disorders like metabolic syndrome and diabetes. An altered cellular metabolism has been recognized as one of the hallmarks of cancer, since malignant cells can divert flux through their metabolic pathways (glycolysis, pentose phosphate pathway, Krebs cycle, etc.) to increase macromolecule and organelle biosynthesis and maintain cellular proliferation. Recent research has associated some of these metabolic changes, particularly in mitochondria, to the production of reactive oxygen species (ROS), reactive oxygen by-products with strong oxidation and signaling functions.

This Special Issue welcomes submissions of original research and reviews from diverse areas of cellular biology and biomedical research fields concerned with metabolic and ROS functions and alterations in human diseases, with the purpose of stimulating intriguing perspectives in the discipline.

Dr. Paola Maycotte
Dr. Álvaro Marín-Hernández
Prof. Dr. Annie Joubert
Guest Editors

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 250 words) can be sent to the Editorial Office for assessment.

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-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Metabolites 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

  • cancer
  • ROS
  • glycolysis
  • mitochondria autophagy
  • antioxidant system
  • glutathione
  • oxidative phosphorylation

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Published Papers (1 paper)

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Review

42 pages, 2644 KB  
Review
Nicotinamide Mononucleotide Adenylyltransferase 1 and NAD+ Homeostasis in Neuroprotection and Aging
by You Sun, Bowei Li and Zhengjiang Qian
Metabolites 2026, 16(8), 597; https://doi.org/10.3390/metabo16080597 - 21 Aug 2026
Abstract
Nicotinamide adenine dinucleotide (NAD+) is a fundamental metabolic cofactor and signaling molecule that supports redox reactions, DNA repair, chromatin regulation, stress adaptation, inflammation, and neuronal maintenance. Age-associated NAD+ decline has been implicated in brain aging and neurodegenerative disorders, but the [...] Read more.
Nicotinamide adenine dinucleotide (NAD+) is a fundamental metabolic cofactor and signaling molecule that supports redox reactions, DNA repair, chromatin regulation, stress adaptation, inflammation, and neuronal maintenance. Age-associated NAD+ decline has been implicated in brain aging and neurodegenerative disorders, but the causal node and limiting compartment differ across tissues and disease states. Nicotinamide mononucleotide adenylyltransferase 1 (NMNAT-1) catalyzes the final step in NAD+ biosynthesis and represents the major nuclear isoform of the mammalian NMNAT family. Direct human genetic evidence establishes NMNAT-1 as a causal gene in inherited retinal degeneration, whereas evidence linking endogenous NMNAT-1 to broader brain aging or sporadic neurodegeneration is mainly convergent preclinical, preliminary, or indirect. Beyond NAD+ synthesis, biochemical and Drosophila studies suggest possible chaperone-like and proteostasis-supporting functions, but a separable NAD+-independent function of endogenous mammalian NMNAT-1 has not yet been established in vivo. Here, we review the molecular structure, localization, and regulation of NMNAT-1, emphasizing calibrated distinctions among catalytic nuclear NAD+ supply, engineered axonal protection, pathway-adjacent NAD+ interventions, and putative non-catalytic protection. We further discuss how NMNAT-1 dysfunction may contribute to aging-associated genomic instability, neuroinflammation, synaptic impairment, retinal degeneration, selected neurodegenerative models, and glioma biology. Finally, we evaluate therapeutic strategies targeting NMNAT-1 and NAD+ pathways, noting that no human trial has yet established efficacy for an NMNAT-1-directed neurological therapy. A compartment-aware and evidence-stratified view is therefore essential for translating NMNAT-1 biology into interventions for age-related neural disease. Full article
(This article belongs to the Special Issue Reactive Oxygen Species and Metabolic Dysregulation: From Bench to Bedside)
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