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: 30 September 2025 | Viewed by 1130

Special Issue Editor


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Guest Editor
Department of Physiology, University of Valencia, 46010 Valencia, Spain
Interests: aging; frailty; nutritional interventions; neuroprotection
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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

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Keywords

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

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Published Papers (1 paper)

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Research

17 pages, 2157 KiB  
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
Viewed by 619
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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