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Antioxidants
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Exploring New Frontiers in Oxidative Stress and Antioxidant Research: From...
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Exploring New Frontiers in Oxidative Stress and Antioxidant Research: From Model Organisms to Human Disease

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 July 2026 | Viewed by 14586

Special Issue Editors

Dr. Marcello Ziosi

E-Mail Website
Guest Editor
New York Genome Center, New York, NY 10013, USA
Interests: developmental genetics; genomics; mitochondria; cell signaling
Dr. Gaetano Santulli

E-Mail Website
Guest Editor
1. Departments of Medicine and Molecular Pharmacology, Wilf Family Cardiovascular Research Institute, Fleischer Institute for Diabetes and Metabolism (FIDAM), Einstein Institute for Aging Research, Einstein-Mount Sinai Diabetes Research Center (ES-DRC), Institute for Neuroimmunology and Inflammation (INI), Albert Einstein College of Medicine and Montefiore Hospital, New York, NY, USA
2. International Translational Research and Medical Education (ITME) Consortium, Academic Research Unit, Department of Advanced Biomedical Sciences, Federico II University, Naples, Italy
Interests: cardiology; hypertension; restenosis; heart failure; myocardial infarction; endothelial dysfunction; mitochondria; diabetes; microRNAs; insulin resistance; atherosclerosis; thrombosis; cardiac hypertrophy; pancreatic beta cell function; insulin release
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Oxidative stress plays a critical role in the pathogenesis of numerous human diseases, including cancer, neurological disorders, cardiometabolic conditions, and aging. Understanding the intricate mechanisms regulating oxidative stress and the homeostatic antioxidant response is essential for developing innovative therapeutic interventions.

Insights gained from model organisms offer valuable perspectives on the molecular and cellular processes underlying oxidative stress, paving the way for novel translational approaches in human disease research. This Special Issue aims to highlight recent advancements in oxidative stress and antioxidant research using model organisms with direct relevance to human health.

We welcome contributions focusing on cellular processes such as cell cycle regulation, intercellular communication, and cell death—key pathways implicated in disease progression. Special emphasis will be placed on studies employing cutting-edge, high-throughput omics technologies, including transcriptomics, single-cell genomics, metabolomics, and proteomics. Additionally, novel strategies for the targeted delivery of antioxidant-based therapies will be of particular interest.

By integrating findings from diverse model systems, this Special Issue seeks to foster a deeper understanding of oxidative stress-related pathophysiology and drive the development of effective therapeutic strategies for human diseases.

Dr. Marcello Ziosi
Dr. Gaetano Santulli
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-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Antioxidants 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 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

  • oxidative stress
  • antioxidant therapeutics
  • cell death and survival pathways
  • cellular signaling networks
  • gene regulation and expression

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Published Papers (6 papers)

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Research

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17 pages, 2007 KB  
Article
A Nutraceutical Approach for Hypertension: Randomized Controlled Trial of Grape Pomace Extract and L-Arginine
by Federico Abate, Elisabetta Schiano, Mariano Stornaiuolo, Fabrizia Guerra, Anna Terracciano, Gaetano Piccinocchi, Eugenio Caradonna, Fulvio Ferrara, Gian Carlo Tenore and Ettore Novellino
Antioxidants 2026, 15(3), 329; https://doi.org/10.3390/antiox15030329 - 5 Mar 2026
Viewed by 926
Abstract
Hypertension remains a major global health challenge, and pharmacological therapy is often constrained by tolerability issues. Adjunctive approaches targeting the nitric oxide synthase and soluble guanylate cyclase–cyclic guanosine monophosphate (sGC–cGMP) pathway may offer additional benefits. This study investigated the efficacy and safety of [...] Read more.
Hypertension remains a major global health challenge, and pharmacological therapy is often constrained by tolerability issues. Adjunctive approaches targeting the nitric oxide synthase and soluble guanylate cyclase–cyclic guanosine monophosphate (sGC–cGMP) pathway may offer additional benefits. This study investigated the efficacy and safety of a nutraceutical formulation combining grape pomace extract (Taurisolo®) and L-arginine in patients with grade 1 and grade 2 hypertension. The formulation was designed to enhance nitric oxide (NO) bioavailability and support sGC–cGMP signaling. Taurisolo®, a polyphenol-rich extract, is known for its antioxidant and endothelial-protective properties, while L-arginine serves as the physiological substrate for endothelial NO synthase. Clinical outcomes included blood pressure changes, renal function parameters, and health-related quality of life assessed through the SF-12 questionnaire. Supplementation with Taurisolo® plus L-arginine resulted in significant and sustained reductions in systolic and diastolic blood pressure, with renal function remaining stable throughout the study. Participants also reported meaningful improvements in perceived health, emotional well-being, vitality, and social functioning. The intervention was well tolerated, with no major adverse effects. These findings support the potential of Taurisolo® combined with L-arginine as a safe and effective adjunctive strategy to conventional antihypertensive therapy, warranting further mechanistic investigation. Full article
(This article belongs to the Special Issue Exploring New Frontiers in Oxidative Stress and Antioxidant Research: From Model Organisms to Human Disease)
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18 pages, 2561 KB  
Article
Hydroxytyrosol Modulates Arachidonic Acid Metabolism and Purine Catabolism in Individuals with Prediabetes: An Untargeted Metabolomics Study in a Randomized Controlled Trial
by Ignacio Moratilla-Rivera, Elisa Fernández-Millán, Jara Pérez-Jiménez, Sonia Ramos, Óscar Yanes, Jordi Capellades, Raquel Mateos and María Ángeles Martín
Antioxidants 2026, 15(3), 317; https://doi.org/10.3390/antiox15030317 - 3 Mar 2026
Cited by 1 | Viewed by 870
Abstract
Background: Hydroxytyrosol (HT) is a phenolic compound found in extra virgin olive oil that modulates oxidative and inflammatory status. However, clinical trials evaluating HT as a stand-alone supplement remain scarce, and its underlying mechanisms and pathway modulation are not yet fully understood. This [...] Read more.
Background: Hydroxytyrosol (HT) is a phenolic compound found in extra virgin olive oil that modulates oxidative and inflammatory status. However, clinical trials evaluating HT as a stand-alone supplement remain scarce, and its underlying mechanisms and pathway modulation are not yet fully understood. This study aimed to investigate the metabolic effects of HT supplementation in individuals with overweight and prediabetes using an untargeted metabolomics approach. Methods: An untargeted liquid chromatography–mass spectrometry (LC–MS)-based metabolomics analysis was performed on serum samples from 49 participants with overweight and prediabetes enrolled in a randomized controlled trial. Participants received either HT (15 mg/day for 16 weeks; n = 24) or placebo (n = 25). Global metabolomic profiling was used to compare metabolic changes between the two groups. Results: HT supplementation induced a distinct metabolic profile compared with placebo. Participants in the HT group showed reduced levels of nitrogenous base derivatives and arachidonic acid, together with increased concentrations of phosphatidylcholines, lysophosphatidylcholines and sphingomyelins. These alterations suggest modulation of two key metabolic pathways including purine degradation and arachidonic acid metabolism. Conclusions: These findings provide mechanistic insights into the biological effects of HT and support the integration of metabolomics and multi-omics approaches in future clinical studies to validate these pathways in larger populations. Full article
(This article belongs to the Special Issue Exploring New Frontiers in Oxidative Stress and Antioxidant Research: From Model Organisms to Human Disease)
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17 pages, 2145 KB  
Article
Redox-Related Genetic and Biological Ageing Signals in Rapid Pain Progression of Knee Osteoarthritis: A Hypothesis-Generating Analysis in the Osteoarthritis Initiative
by Francisco J. Blanco, Natividad Oreiro, Jorge Vázquez-García, Antonio Morano-Torres, Sara Relaño, Laura Martínez-Sotodosos, Diana M. Noriega-Cobo, Fátima Otero-Fariña, Alejandro Mosquera, Jose L. Fernández and Ignacio Rego-Pérez
Antioxidants 2026, 15(2), 266; https://doi.org/10.3390/antiox15020266 - 21 Feb 2026
Viewed by 685
Abstract
Rapid pain progression in knee osteoarthritis (OA) is heterogeneous and may reflect redox-related mechanisms. We performed an exploratory analysis in Osteoarthritis Initiative (OAI) participants, combining nuclear genome-wide association, mitochondrial DNA (mtDNA) haplogroups, and leukocyte telomere length. Rapid pain progression was defined using the [...] Read more.
Rapid pain progression in knee osteoarthritis (OA) is heterogeneous and may reflect redox-related mechanisms. We performed an exploratory analysis in Osteoarthritis Initiative (OAI) participants, combining nuclear genome-wide association, mitochondrial DNA (mtDNA) haplogroups, and leukocyte telomere length. Rapid pain progression was defined using the rescaled Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) for pain (0–100) within 24-month windows. An additive genome-wide association study (GWAS) in 2946 participants tested 7,762,204 imputed variants, adjusting for age, sex, body mass index (BMI) and three principal components. Haplogroups were analysed in 3357 participants, and telomere length (telomere-to-single-copy gene, T/S, ratio) was analysed in 301 participants. No variant reached genome-wide significance (p < 5 × 10−8), but six loci were suggestive (p < 5 × 10−6), with minimal inflation (λ = 0.995). mtDNA haplogroup H was nominally associated with rapid pain progression (odds ratio, OR = 1.179, p = 0.023). Rapid pain progressors had shorter baseline telomeres (0.825 ± 0.268 vs. 0.985 ± 0.375; p < 0.001), and telomere length was inversely associated with progression (OR per 1-unit T/S = 0.260, p = 0.007). These preliminary, hypothesis-generating findings are compatible with a redox-related interpretation of rapid pain progression and require external validation in independent cohorts, while providing candidates for future mechanistic studies. Full article
(This article belongs to the Special Issue Exploring New Frontiers in Oxidative Stress and Antioxidant Research: From Model Organisms to Human Disease)
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Review

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31 pages, 1457 KB  
Review
Ferroptosis in Human Diseases: Fundamental Roles and Emerging Therapeutic Perspectives
by Ilaria Artusi, Michela Rubin, Giovanni Cravin and Giorgio Cozza
Antioxidants 2025, 14(12), 1411; https://doi.org/10.3390/antiox14121411 - 26 Nov 2025
Cited by 8 | Viewed by 5318
Abstract
Ferroptosis is a novel iron-sensitive subtype of regulated cell death (RCD), persisting under extreme lipid peroxidation and iron/redox imbalances. Unlike apoptosis, necroptosis, and pyroptosis, ferroptosis is a signaling-driven process mediated through iron metabolism imbalance, polyunsaturated fatty acid (PUFA) exceeding oxidation, and defects in [...] Read more.
Ferroptosis is a novel iron-sensitive subtype of regulated cell death (RCD), persisting under extreme lipid peroxidation and iron/redox imbalances. Unlike apoptosis, necroptosis, and pyroptosis, ferroptosis is a signaling-driven process mediated through iron metabolism imbalance, polyunsaturated fatty acid (PUFA) exceeding oxidation, and defects in its protective systems like Xc-/GSH/GPx4. Specifically, this review establishes that iron-driven ferroptosis is a central underlying pathomechanistic factor in a broad range of human diseases. Significantly, whether its modulation is therapeutic, it is entirely conditional on the specific disease context. Thus, its induction can provide a promising antidote for destructive cancer cells when conjoined with immuno-therapies to boost anticancer immunity. Conversely, iron-mediated ferroptosis suppression is a key factor in countering destructive changes in a whole range of degenerative and acute injuries. Current therapeutic approaches include iron chelators, lipid oxidation inhibitors, GPx4 activators, natural and active compounds, and novel drug delivery systems. However, against all odds and despite its intense therapeutic promise, its translation into a practical medicinal strategy faces many difficulties. Thus, a therapeutic agent specifically focused on its modulation is still lacking. The availability of selective biologic markers is a concern. The challenges in the direct pathologic identification of ferroptosis in a complex in vivo systemic scenario remain. Current avenues for its future development are pathogen infections, the discovery of novel regulating factors, and novel approaches to personalized medicine centered on its organ-level in vivo signatures. Full article
(This article belongs to the Special Issue Exploring New Frontiers in Oxidative Stress and Antioxidant Research: From Model Organisms to Human Disease)
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18 pages, 1837 KB  
Review
Emerging and Versatile Non-Mammalian Model Organisms for Studying the In Vivo Antioxidant Properties of Food-Derived Bioactive Compounds
by Alejandra Miranda-Carrazco, Verenice Torres-Salas, Rosy G. Cruz-Monterrosa, Monzerrat Rosas-Espejel, Ildefonso Guerrero-Encinas, Javier N. González-González, Luis Quihui-Cota, Andrea M. Liceaga and José E. Aguilar-Toalá
Antioxidants 2025, 14(9), 1127; https://doi.org/10.3390/antiox14091127 - 18 Sep 2025
Cited by 2 | Viewed by 1452
Abstract
In recent years, there has been increased attention to exploring non-mammalian model organisms to study the antioxidant properties of bioactive compounds. These models include both unicellular organisms, such as Escherichia coli and Saccharomyces cerevisiae, and multicellular organisms, such as Caenorhabditis elegans, Drosophila [...] Read more.
In recent years, there has been increased attention to exploring non-mammalian model organisms to study the antioxidant properties of bioactive compounds. These models include both unicellular organisms, such as Escherichia coli and Saccharomyces cerevisiae, and multicellular organisms, such as Caenorhabditis elegans, Drosophila melanogaster, and Danio rerio. In particular, multicellular models have emerged as promising systems due to their ease of establishing systems and maintenance, short duration of experiments, ease of genetic manipulation and genome-wide screening, availability as off-the-shelf models, safety, and cost-effectiveness. Notably, these organisms share a high degree of gene homology with humans, ranging from 65% to 84%, which positions them as powerful platforms for investigating human disease mechanisms. These advantages make them attractive candidates for investigating the potential health benefits of various bioactive compounds before resorting to mammalian models. This review delves into the rationale for utilizing these emerging non-mammalian model organisms during preliminary stages of research, emphasizing their distinct advantages over traditional mammalian models. It also highlights their significant contributions to advancing our understanding of the antioxidant mechanisms of bioactive compounds, shedding light on their potential therapeutic implications for human health. By leveraging these models, researchers can efficiently screen and validate bioactive compounds, laying a robust foundation for subsequent translational studies in mammalian systems. Full article
(This article belongs to the Special Issue Exploring New Frontiers in Oxidative Stress and Antioxidant Research: From Model Organisms to Human Disease)
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36 pages, 757 KB  
Review
Oxidative Stress in the Pathophysiology of Chronic Venous Disease: An Overview
by Sonia Rațiu, Mihaela I. Mariș, Adina V. Furdui-Lința, Laurențiu V. Sima, Tiberiu I. Bratu, Adrian Sturza, Danina M. Muntean and Octavian M. Crețu
Antioxidants 2025, 14(8), 989; https://doi.org/10.3390/antiox14080989 - 12 Aug 2025
Cited by 8 | Viewed by 4308
Abstract
Chronic venous disease (CVD) and its major manifestation, varicose veins (VV) of the lower limbs, is a common, multifactorial disease that affects a significant percentage of adult and elderly people worldwide. Its prevalence has been constantly increasing with the aging of the population [...] Read more.
Chronic venous disease (CVD) and its major manifestation, varicose veins (VV) of the lower limbs, is a common, multifactorial disease that affects a significant percentage of adult and elderly people worldwide. Its prevalence has been constantly increasing with the aging of the population and, particularly, with the obesity pandemic (hence, the term ‘phlebesity’). The major pathophysiological mechanisms that are potentiating each other in a vicious cycle, leading to chronic venous hypertension, are represented by endothelial dysfunction, chronic inflammation, impaired hemodynamics, and venous wall remodeling. Oxidative stress is another pathomechanism responsible for CVD and its complications, with the increased generation of reactive oxygen species and decreased antioxidant defense being reported to contribute to VV formation. Herein, we present evidence for the role of impaired redox homeostasis as pathophysiological mechanism responsible for chronic local and systemic oxidative stress in patients with CVD. Full article
(This article belongs to the Special Issue Exploring New Frontiers in Oxidative Stress and Antioxidant Research: From Model Organisms to Human Disease)
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