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Antioxidants
Special Issues
Oxidative Stress in Age-Related Diseases
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Oxidative Stress in Age-Related Diseases

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 May 2026 | Viewed by 4089

Special Issue Editor

Dr. Gloria Olaso-Gonzalez

E-Mail Website
Guest Editor
Department of Physiology, University of Valencia, 46010 Valencia, Spain
Interests: aging; frailty; nutritional interventions; neuroprotection
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The understanding of the role of free radicals in aging has undergone significant revisions. Traditionally, the mitochondrial free radical theory of aging (FRTA), proposed by Harman in 1965, implicated reactive oxygen species (ROS) as the primary culprits in cellular aging due to their production exceeding the body’s antioxidant defenses. However, studies in various animal models have revealed no consistent correlation between ROS levels and lifespan, prompting a paradigm shift in our comprehension of ROS functions. It is now recognized that ROS play a pivotal signaling role, activating compensatory homeostatic responses within cells. During aging, elevated ROS levels initially trigger these protective mechanisms, but beyond a certain threshold, they contribute to cellular damage and exacerbate age-related pathologies. Experimental data have demonstrated that oxidative damage correlates more closely with frailty than with chronological age, leading to the formulation of the free radical theory of frailty.

This Special Issue explores the interplay between redox modulation and age-related diseases, with a particular focus on frailty. By integrating findings from both experimental animal models and human cohorts, we aim to advance our understanding of oxidative stress and its role in the progression of diseases associated with aging and frailty, paving the way for innovative therapeutic strategies.

Dr. Gloria Olaso-Gonzalez
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 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

  • aging
  • age-related diseases
  • frailty
  • oxidative stress
  • reductive stress
  • redox homeostasis
  • antioxidants

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Published Papers (3 papers)

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Research

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14 pages, 781 KB  
Article
Associations Between Gut Microbiota and Mitochondrial Metabolites, with Growth Differentiation Factor-15 as a Marker of Oxidative Stress in Heart Failure vs. Healthy Ageing
by Konstantinos Prokopidis, Adam Burke, Beyza Gulsah Altinpinar, Sima Jalali Farahani, Omid Khaiyat, Gregory Y. H. Lip, Rajiv Sankaranarayanan, Vanja Pekovic-Vaughan, Howbeer Muhamadali and Masoud Isanejad
Antioxidants 2026, 15(2), 199; https://doi.org/10.3390/antiox15020199 - 2 Feb 2026
Abstract
Growth differentiation factor-15 (GDF-15) is an established marker of oxidative stress and a general stress-response mitokines. In this study, we aim to investigate the association of GDF-15 with the metabolic signature of gut and mitochondrial activity in HF and ageing population. A total [...] Read more.
Growth differentiation factor-15 (GDF-15) is an established marker of oxidative stress and a general stress-response mitokines. In this study, we aim to investigate the association of GDF-15 with the metabolic signature of gut and mitochondrial activity in HF and ageing population. A total of 25 HF (67.9 ± 10.0 years) and 29 age-matched healthy participants (HPs) (67.8 ± 11.1 years) were recruited and underwent detailed body composition assessment via dual X-ray absorptiometry; total fat mass and appendicular lean soft tissue index (ALSTI/body mass index (BMI)) were calculated. Utilizing semi-targeted Gas Chromatography–Mass Spectrometry on fasting plasma, a panel of gut microbial-derived (e.g., hippuric acid, indole derivatives, and sarcosine) and tricarboxylic acid cycle metabolites was identified. Results showed higher GDF-15 tertiles were associated with greater HF prevalence, fat mass, NT-proBNP, and TNF-α (p < 0.05). Gut-derived metabolites exhibited phenotype-specific patterns; 3-hydroxyindole predicted higher fat mass in HP; hippuric acid was inversely related in HF; and sarcosine correlated with GDF-15 only in HP. In HF, GDF-15 was strongly driven by pyruvic and fumaric acid, indicating disease-specific mitochondrial stress. In conclusion, these observed associations could be evaluated in future mechanistic studies as sensitive biomarkers of systemic oxidative stress markers, informing potential microbiome-targeted therapeutic avenues. Full article
(This article belongs to the Special Issue Oxidative Stress in Age-Related Diseases)
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17 pages, 2157 KB  
Article
Antioxidant, Osteogenic, and Neuroprotective Effects of Homotaurine in Aging and Parkinson’s Disease Models
by Arianna Minoia, Francesca Cristiana Piritore, Silvia Bolognin, João Pessoa, Bruno Bernardes de Jesus, Natascia Tiso, Maria Grazia Romanelli, Jens Christian Schwamborn, Luca Dalle Carbonare and Maria Teresa Valenti
Antioxidants 2025, 14(3), 249; https://doi.org/10.3390/antiox14030249 - 21 Feb 2025
Cited by 1 | Viewed by 2322
Abstract
Aging is associated with the accumulation of cellular damage due to oxidative stress and chronic low-grade inflammation, collectively referred to as “inflammaging”. This contributes to the functional decline in various tissues, including the brain and skeletal system, which closely interplay. Mesenchymal stem cells [...] Read more.
Aging is associated with the accumulation of cellular damage due to oxidative stress and chronic low-grade inflammation, collectively referred to as “inflammaging”. This contributes to the functional decline in various tissues, including the brain and skeletal system, which closely interplay. Mesenchymal stem cells (MSCs), known for their regenerative potential and ability to modulate inflammation, offer a promising therapeutic approach to counteract aging-related declines. In this study, we investigated the effects of homotaurine (a small molecule with neuroprotective properties) on MSCs and its effects on osteogenesis. We found that homotaurine treatment significantly reduced reactive oxygen species (ROS) levels, improved MSC viability, and modulated key stress response pathways, including the sestrin 1 and p21 proteins. Furthermore, homotaurine promoted osteogenesis and angiogenesis in zebrafish models by enhancing the expression of critical osteogenesis-associated genes, such as those coding for β-catenin and Runt-related transcription factor 2 (Runx2), and increasing the levels of the kinase insert domain receptor-like angiogenesis marker in aged zebrafish. In Parkinson’s disease models using patient-specific midbrain organoids with the leucine-rich repeat kinase 2 G2019S mutation, homotaurine treatment enhanced β-catenin expression and reduced ROS levels, highlighting its potential to counteract the oxidative stress and dysfunctional signaling pathways associated with neurodegeneration. Our findings suggest that homotaurine not only offers neuroprotective benefits but also holds promise as a dual-target therapeutic strategy for enhancing both neuronal and bone homeostasis in aging and neurodegenerative diseases. Full article
(This article belongs to the Special Issue Oxidative Stress in Age-Related Diseases)
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Review

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29 pages, 1362 KB  
Review
Redox Regulation of Complement Pathway Activation in Aging and Related Diseases
by Shirin Ferdowsi, Srividya Arjuna, Sudharshan SJ and Rahima Zennadi
Antioxidants 2026, 15(1), 29; https://doi.org/10.3390/antiox15010029 - 24 Dec 2025
Viewed by 777
Abstract
Aging is a complex degenerative process characterized by the accumulation of molecular damage and a heightened susceptibility to disease. The oxidative stress theory of aging identifies endogenous reactive oxygen species (ROS) as primary drivers of this cellular deterioration. This review provides a comprehensive [...] Read more.
Aging is a complex degenerative process characterized by the accumulation of molecular damage and a heightened susceptibility to disease. The oxidative stress theory of aging identifies endogenous reactive oxygen species (ROS) as primary drivers of this cellular deterioration. This review provides a comprehensive analysis of the critical, yet underappreciated, interplay between oxidative stress and the complement system, a powerful effector of innate immunity. We detail the mechanistic pathways through which redox imbalance directly activates complement components and, conversely, how complement activation amplifies oxidative stress, creating a vicious cycle that accelerates tissue damage. A central focus is placed on how this redox–complement axis contributes to the pathophysiology of age-related conditions, including neurodegenerative, cardiovascular, and metabolic diseases. Furthermore, the review explores emerging therapeutic strategies that target this interaction, highlighting the potential of antioxidant and complement-inhibitory approaches to disrupt this cycle and promote healthy aging. By synthesizing current evidence, this work underscores the significance of the redox–complement network as a key mechanistic link in aging and its associated diseases. Full article
(This article belongs to the Special Issue Oxidative Stress in Age-Related Diseases)
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