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Antioxidants
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The Role of Oxidative Stress in Age-Related and Degenerative Eye...
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The Role of Oxidative Stress in Age-Related and Degenerative Eye 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 July 2026 | Viewed by 6654

Special Issue Editor

Dr. Ting Zhang

E-Mail Website
Guest Editor
Save Sight Institute, Faculty of Medicine and Health, The University of Sydney, Sydney, NSW 2006, Australia
Interests: retinal diseases; age-related macular degeneration (AMD); Müller glia; oxidative stress; mitochondrial dysfunction; macular vulnerability; retinal metabolism
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Oxidative stress plays a central role in the development and progression of many eye diseases, especially those associated with aging and neurodegeneration. As reactive oxygen species build up and redox balance is lost, the resulting damage to retinal structures contributes to vision decline in individuals with conditions such as age-related macular degeneration (AMD), glaucoma, diabetic retinopathy, and cataracts.

This Special Issue of Antioxidants brings together current insights into how oxidative stress drives pathology in the aging eye. We are particularly interested in how redox imbalance disrupts key cell types, like the cells of the retinal pigment epithelium, photoreceptors, and ganglion cells, and how these changes intersect with inflammation, mitochondrial dysfunction, protein misfolding, and impaired autophagy.

We invite contributions of original research papers and reviews that explore these mechanisms at any scale, from molecular to systemic. We especially welcome studies on antioxidant therapies, redox-sensitive pathways, gene–environment interactions, emerging biomarkers, and models that advance translational potential.

In addition, we strongly encourage contributions that highlight the application of new technologies in vision science research. This includes the use of artificial intelligence (AI) and machine learning to analyze high-dimensional omics data, predict disease progression, identify novel therapeutic targets, and uncover hidden patterns in redox-related cellular responses. Studies integrating AI with imaging, bioinformatics, or experimental models to address oxidative stress in ocular diseases are particularly welcome.

By drawing attention to this common pathological phenomenon and embracing cutting-edge analytical tools, we hope to deepen understanding of this issue and accelerate progress toward therapies that can meaningfully alter the course of age-related eye disease.

Dr. Ting Zhang
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

  • oxidative stress
  • age-related macular degeneration
  • retinal degeneration
  • reactive oxygen species
  • redox signaling
  • mitochondrial dysfunction
  • antioxidant therapy
  • artificial intelligence
  • multi-omics
  • biomarkers
  • vision science

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Published Papers (5 papers)

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Research

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21 pages, 17866 KB  
Article
Nostoc commune Extract Attenuates Oxidative Stress and Neuroinflammation in Ischemic Optic Neuropathy Through PI3K/AKT/mTOR Signaling
by Jia-Ying Chien, Wei-Hsun Chan, Mei-Ling Peng, Siu-Fung Chau, Hsien-Yang Tsai, Shi-Huang Lee, Yu-Chen Chen, Wai-Man Cheang and Shun-Ping Huang
Antioxidants 2026, 15(5), 541; https://doi.org/10.3390/antiox15050541 - 24 Apr 2026
Viewed by 253
Abstract
Non-arteritic anterior ischemic optic neuropathy (NAION) is a leading cause of sudden vision loss, yet no effective therapy exists to preserve retinal ganglion cells (RGCs) after ischemic injury. Nostoc commune (NC), an edible cyanobacterium with established antioxidant and anti-inflammatory activities, has emerged as [...] Read more.
Non-arteritic anterior ischemic optic neuropathy (NAION) is a leading cause of sudden vision loss, yet no effective therapy exists to preserve retinal ganglion cells (RGCs) after ischemic injury. Nostoc commune (NC), an edible cyanobacterium with established antioxidant and anti-inflammatory activities, has emerged as a potential functional bioresource with relevance to ocular health. Here, we investigated the therapeutic effects of a crude aqueous extract of NC using a rodent model of anterior ischemic optic neuropathy (rAION). NC treatment significantly improved RGC survival, reduced apoptosis, attenuated macrophage and microglial activation (ED-1, Iba1), suppressed proinflammatory cytokine expression (IL-6), enhanced the reparative marker Ym1+2, and preserved optic-nerve myelination. Functionally, NC administration restored visual signaling as demonstrated by improved Flash Visual Evoked Potential amplitudes. Immunoblot analysis showed increased phosphorylation of PI3K/AKT/mTOR/p70S6K signaling components in retinal tissue following NC treatment. Proteomic profiling further demonstrated that NC extract comprises a coordinated repertoire of phycobiliproteins, antioxidant enzymes, and stress-response proteins that may collectively contribute to its biological effects. Together, these findings suggest that Nostoc commune extract may serve as a promising functional food-derived candidate for protecting RGCs and preserving visual function following ischemic optic neuropathy. Further studies are required to identify its active constituents, optimize formulation strategies, and evaluate its translational potential. Full article
(This article belongs to the Special Issue The Role of Oxidative Stress in Age-Related and Degenerative Eye Diseases)
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18 pages, 13495 KB  
Article
HDGF Protects Retinal Pigment Epithelium from Glyoxal-Induced Ferroptosis via SIRT1/PGC-1α/Nrf2 Pathway
by Heng-Dao Lin, Rong-Kung Tsai, Yao-Tseng Wen and Pei-Kang Liu
Antioxidants 2025, 14(12), 1434; https://doi.org/10.3390/antiox14121434 - 28 Nov 2025
Viewed by 1357
Abstract
Age-related macular degeneration (AMD) is driven in part by the accumulation of reactive metabolites like glyoxal (GO), which induces retinal pigment epithelium (RPE) degeneration. Here, we demonstrate that GO triggers ferroptosis in human ARPE-19 cells, as characterized by iron-dependent lipid peroxidation, glutathione depletion, [...] Read more.
Age-related macular degeneration (AMD) is driven in part by the accumulation of reactive metabolites like glyoxal (GO), which induces retinal pigment epithelium (RPE) degeneration. Here, we demonstrate that GO triggers ferroptosis in human ARPE-19 cells, as characterized by iron-dependent lipid peroxidation, glutathione depletion, and reactive oxygen species (ROS) accumulation. This ferroptotic cell death is coupled with profound mitochondrial dysfunction, featuring network fragmentation and the downregulation of the key regulators MFN2, PGC-1α, and SIRT1. We identify hepatoma-derived growth factor (HDGF) as a potent protector against GO-induced damage. HDGF operates through a dual mechanism: it activates the p38 MAPK/AKT and SIRT1/PGC-1α axes to restore mitochondrial biogenesis and homeostasis, while concurrently enhancing the glutathione/GPX4 antioxidant system to suppress ferroptosis. This cytoprotective action is mediated via the PGC-1α/Nrf2 pathway, which integrates the enhancement of antioxidant defenses with the preservation of mitochondrial integrity. Our findings establish HDGF as a novel therapeutic agent for AMD, uniquely capable of concurrently targeting the interconnected pathways of ferroptosis and mitochondrial dysfunction, thereby addressing a critical unmet need in retinal disease treatment. Full article
(This article belongs to the Special Issue The Role of Oxidative Stress in Age-Related and Degenerative Eye Diseases)
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Review

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18 pages, 718 KB  
Review
Saffron as a Retinal Neuroprotectant: A Narrative Review of Preclinical Studies and Clinical Results
by Maria Anna Maggi, Rocco Mastromartino, Marco Piccardi, Angelo Maria Minnella, Dario Marangoni, Stefano Di Marco, Benedetto Falsini and Silvia Bisti
Antioxidants 2026, 15(4), 501; https://doi.org/10.3390/antiox15040501 - 17 Apr 2026
Viewed by 1209
Abstract
The present narrative review reports the main preclinical and clinical results obtained by using supplementation of saffron or its pure components in neurodegeneration, with special emphasis on age-related macular degeneration. Beyond that, this article will address shared pathways between neurodegenerative diseases of the [...] Read more.
The present narrative review reports the main preclinical and clinical results obtained by using supplementation of saffron or its pure components in neurodegeneration, with special emphasis on age-related macular degeneration. Beyond that, this article will address shared pathways between neurodegenerative diseases of the eye and the brain. It will be shown that saffron treatment might counteract oxidative damage in the retina and brain, as well as inflammation and inflammatory mediators that induce neuronal degeneration and death. The ways of action are multiple, and saffron chemical components appear to act in a synergistic manner, inducing tissue resilience. These effects critically depend upon the saffron chemical composition and structure. A well-defined ratio among molecules is linked to a patented batch known as Repron® and offers the maximum protection against neurodegeneration. Full article
(This article belongs to the Special Issue The Role of Oxidative Stress in Age-Related and Degenerative Eye Diseases)
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35 pages, 3144 KB  
Review
Ferroptosis-Mediated Cell-Specific Damage: Molecular Cascades and Therapeutic Breakthroughs in Diabetic Retinopathy
by Yan Chen, Rongyu Wang, Nannan Zhang and Liangzhi Xu
Antioxidants 2026, 15(1), 1; https://doi.org/10.3390/antiox15010001 - 19 Dec 2025
Viewed by 2078
Abstract
Diabetic retinopathy (DR), a leading cause of vision loss in diabetic patients, involves complex pathological mechanisms including neurodegeneration, microvascular damage, inflammation, and oxidative stress. Recent studies have identified ferroptosis—a ferrodependent cell death mechanism—as playing a pivotal role in DR development. Existing evidence indicates [...] Read more.
Diabetic retinopathy (DR), a leading cause of vision loss in diabetic patients, involves complex pathological mechanisms including neurodegeneration, microvascular damage, inflammation, and oxidative stress. Recent studies have identified ferroptosis—a ferrodependent cell death mechanism—as playing a pivotal role in DR development. Existing evidence indicates that oxidative stress and mitochondrial dysfunction induced by hyperglycemia may contribute to retinal damage through the ferroptosis pathway in DR. Ferroptosis inhibitors such as Ferostatin-1 have demonstrated protective effects against DR in animal models. The core mechanisms of ferroptosis involve iron homeostasis imbalance and lipid peroxidation, with key regulatory pathways including GPX4-dependent and non-dependent mechanisms (such as FSP1-CoQ10). Within the signaling network, Nrf2 inhibits ferroptosis, p53 promotes it, while Hippo/YAP functions are environment-dependent. Non-coding RNAs and epigenetic modifications (e.g., DNA methylation and histone modifications) also participate in regulation. In DR, iron overload, GPX4 dysfunction, and p53 upregulation collectively induce ferroptosis in various types of retinal cells, making these pathways potential therapeutic targets. This review not only elaborates the role of iron metabolism imbalance and ferroptosis pathway in the occurrence and development of DR but also summarizes the new therapeutic approaches of DR targeting ferroptosis pathway. Investigating the relationship between ferroptosis and DR not only helps unravel its core pathophysiological mechanisms but also provides theoretical foundations for developing novel therapeutic approaches. Full article
(This article belongs to the Special Issue The Role of Oxidative Stress in Age-Related and Degenerative Eye Diseases)
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23 pages, 2079 KB  
Review
The Interplay Between the Ubiquitin–Proteasome System and Oxidative Stress: A Future Perspective in Eye Diseases
by Grazia Raffaella Tundo, Gabriele Antonio Zingale, Irene Pandino, Elisa Peroni, Diego Sbardella and Alessio Bocedi
Antioxidants 2025, 14(12), 1475; https://doi.org/10.3390/antiox14121475 - 9 Dec 2025
Viewed by 1134
Abstract
Redox unbalance, a molecular trait common to neurodegenerative conditions and para-physiological processes like aging, is a critical factor in disease development and in exacerbating progression. The mechanism by which redox imbalance perturbs cellular homeostasis is strongly linked to the activity and function of [...] Read more.
Redox unbalance, a molecular trait common to neurodegenerative conditions and para-physiological processes like aging, is a critical factor in disease development and in exacerbating progression. The mechanism by which redox imbalance perturbs cellular homeostasis is strongly linked to the activity and function of the ubiquitin–proteasome system (UPS). The UPS, along with autophagy, is the primary intracellular proteolytic system, regulating targeted proteolysis and removing damaged proteins. Consequently, the UPS serves also as the first line of defense for cellular recovery following exposure to redox stressors. Paradoxically, the composition and function of the UPS can also be negatively targeted by redox unbalance through a vicious cycle. The alterations in redox balance and UPS biological mechanisms are involved in the etiopathogenesis of chronic eye disorders. These disorders encompass a diverse repertoire of pathologies affecting the retinal layers (e.g., age-related macular degeneration, diabetic retinopathy) and the optic nerve (e.g., glaucoma). Nowadays, the comprehension of the interplay between proteostasis and oxidative redox status remains pivotal for identifying new therapeutic approaches. Encouragingly, a number of anti-oxidant compounds have been reported to modulate proteasome activity against redox insults in vitro and in vivo. Furthermore, these compounds provide cytoprotective roles in both in vitro and animal models of eye diseases. Therefore, this review highlights recent research on the interplay of the UPS with oxidative stress in physio-pathological conditions, focusing on the onset and progression of ocular diseases, thereby providing new insights into UPS-oxidative stress interaction. Full article
(This article belongs to the Special Issue The Role of Oxidative Stress in Age-Related and Degenerative Eye Diseases)
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