Oxidative Stress in Metabolic Disorders and Non-Communicable Diseases (NCDs): Molecular Pathways and Genetic Influence

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: 31 March 2026 | Viewed by 3057

Special Issue Editor


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Guest Editor
Dipartimento di Scienze biomediche, Università degli Studi di Sassari, Sassari, Italy
Interests: endothelial cells; gene regulation; reactive oxygen species

Special Issue Information

Dear Colleagues,

Oxidative stress plays a pivotal role in the pathogenesis of various metabolic disorders and non-communicable diseases (NCDs), acting as a critical mediator of cellular damage and dysregulation. The intricate interplay between oxidative stress, molecular pathways, and genetic predisposition has garnered increasing attention in recent years. Reactive oxygen species (ROS), along with their regulatory networks, significantly impact metabolic processes, inflammation, and disease progression, contributing to conditions such as diabetes, cardiovascular diseases, neurodegenerative disorders, and cancer.

We are pleased to announce a call for papers for a Special Issue titled "Oxidative Stress in Metabolic Disorders and Non-Communicable Diseases (NCDs): Molecular Pathways and Genetic Influence". This Special Issue aims to explore the latest advancements in understanding the molecular and genetic mechanisms underlying oxidative stress in these diseases and to identify potential therapeutic targets and strategies.

We invite you to submit your original research, reviews, or methodological studies that address, but are not limited to, the following topics:

  • Molecular mechanisms of oxidative stress in metabolic disorders and NCDs;
  • Genetic susceptibility and epigenetic modifications influencing oxidative stress responses;
  • Crosstalk between oxidative stress and inflammation in disease pathogenesis;
  • Role of antioxidant enzymes and their regulation in cellular homeostasis;
  • Emerging therapies targeting oxidative stress in metabolic and non-communicable diseases;
  • Experimental and computational approaches to study oxidative stress pathways;
  • Biomarkers of oxidative stress and their clinical significance.

Submissions that provide insights into both in vitro and in vivo models or that propose translational approaches to mitigate oxidative stress are highly encouraged.

We look forward to receiving your valuable contributions, which will help advance the understanding of oxidative stress and its impact on metabolic and non-communicable diseases.

Dr. Roberta Giordo
Guest Editor

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Keywords

  • metabolic disorders
  • non-communicable diseases (NCDs)
  • reactive oxygen species (ROS)
  • genetic influence
  • molecular pathways

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Published Papers (2 papers)

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Research

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19 pages, 2344 KB  
Article
PTEN/PKM2/ERα-Driven Glyoxalase 1 Overexpression Sustains PC3 Prostate Cancer Cell Growth Through MG-H1/RAGE Pathway Desensitization Leading to H2O2-Dependent KRIT1 Downregulation
by Dominga Manfredelli, Camilla Torcoli, Marilena Pariano, Guido Bellezza, Tiziano Baroni, Vincenzo N. Talesa, Angelo Sidoni and Cinzia Antognelli
Antioxidants 2025, 14(9), 1120; https://doi.org/10.3390/antiox14091120 - 15 Sep 2025
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Abstract
Glyoxalase 1 (Glo1) functions as a catalyst that neutralizes methylglyoxal (MG), a highly reactive glycating agent predominantly produced during glycolysis—a metabolic pathway upregulated in cancer cells. MG primarily reacts with the amino groups of proteins (especially at arginine residues), leading to the formation [...] Read more.
Glyoxalase 1 (Glo1) functions as a catalyst that neutralizes methylglyoxal (MG), a highly reactive glycating agent predominantly produced during glycolysis—a metabolic pathway upregulated in cancer cells. MG primarily reacts with the amino groups of proteins (especially at arginine residues), leading to the formation of a major advanced glycation end product known as MG-derived hydroimidazolone 1 (MG-H1). We previously demonstrated in PC3 human prostate cancer (PCa) cells that the PTEN/PKM2/ERα axis promotes their aggressive phenotype by regulating the Glo1/MG-H1 pathway. In this study, after confirming our earlier findings, we investigated the downstream mechanisms of the PTEN/PKM2/ERα/Glo1/MG-H1 axis in controlling PC3 cell growth, focusing on the role of RAGE, a high-affinity receptor for MG-H1; hydrogen peroxide (H2O2); and Krev interaction trapped 1 (KRIT1), an emerging tumor suppressor. Using genetic approaches and specific inhibitors/scavengers, we demonstrated that the PTEN/PKM2/ERα/Glo1/MG-H1 axis promotes PC3 cell growth—measured by proliferation and etoposide-induced apoptosis resistance—through a mechanism involving MG-H1/RAGE pathway desensitization that leads to H2O2-mediated KRIT1 downregulation. These findings support and expand the role of PTEN signaling in PCa progression and shed light on novel mechanistic pathways driven by MG-dependent glycative stress, involving KRIT1, in this still incurable stage of the disease. Full article
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Review

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35 pages, 1485 KB  
Review
Role and Functions of Irisin: A Perspective on Recent Developments and Neurodegenerative Diseases
by Aurelio Minuti, Ivana Raffaele, Michele Scuruchi, Maria Lui, Claudia Muscarà and Marco Calabrò
Antioxidants 2025, 14(5), 554; https://doi.org/10.3390/antiox14050554 - 7 May 2025
Cited by 2 | Viewed by 2376
Abstract
Irisin is a peptide derived from fibronectin type III domain-containing protein 5 (FNDC5) and is primarily produced by muscle fibers under the regulation of peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1α) during exercise. Irisin has been the subject of extensive research due to [...] Read more.
Irisin is a peptide derived from fibronectin type III domain-containing protein 5 (FNDC5) and is primarily produced by muscle fibers under the regulation of peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1α) during exercise. Irisin has been the subject of extensive research due to its potential as a metabolic regulator and its antioxidant properties. Notably, it has been associated with protective actions within the brain. Despite growing interest, many questions remain regarding the molecular mechanisms underlying its effects. This review summarizes recent findings on irisin, highlighting its pleiotropic functions and the biological processes and molecular cascades involved in its action, with a particular focus on the central nervous system. Irisin plays a crucial role in neuron survival, differentiation, growth, and development, while also promoting mitochondrial homeostasis, regulating apoptosis, and facilitating autophagy—processes essential for normal neuronal function. Emerging evidence suggests that irisin may improve conditions associated with non-communicable neurological diseases, including Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, frontotemporal dementia, and multiple sclerosis. Given its diverse benefits, irisin holds promise as a novel therapeutic agent for preventing and treating neurological diseases. Full article
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