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Antioxidants
Special Issues
Role of Oxidative Stress in Eye Diseases
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Role of Oxidative Stress in 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: 20 October 2026 | Viewed by 6160

Special Issue Editor

Prof. Dr. Tatsuya Mimura

E-Mail Website
Guest Editor
Department of Ophthalmology, Teikyo University School of Medicine, Tokyo 173-0003, Japan
Interests: ocular regeneration; diabetic retinopathy; corneal diseases

Special Issue Information

Dear Colleagues,

Oxidative stress is recognized as a key factor in the pathophysiology of numerous eye diseases. The eye is particularly vulnerable to oxidative damage due to its high oxygen consumption, continuous exposure to light, and rich content of polyunsaturated fatty acids. Reactive oxygen species (ROS) disrupt cellular homeostasis, induce lipid peroxidation, and damage proteins and DNA, ultimately contributing to the onset and progression of various ocular disorders.

This Special Issue aims to examine the complex role of oxidative stress in the development and progression of eye diseases, including—but not limited to—age-related macular degeneration, diabetic retinopathy, glaucoma, cataracts, and uveitis. We welcome original research articles and comprehensive reviews that explore underlying molecular mechanisms, identify oxidative biomarkers, and assess the efficacy of antioxidants or redox-modulating therapies in promoting ocular health. We encourage the submission of papers that use in vitro, in vivo, and clinical models.

By compiling state-of-the-art research in this area, this Special Issue seeks to deepen our understanding of oxidative stress as a therapeutic target and foster the development of innovative strategies to prevent or mitigate vision loss related to oxidative damage.

Prof. Dr. Tatsuya Mimura
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
  • reactive oxygen species
  • ocular disorders
  • age-related macular degeneration
  • retinopathy
  • glaucoma
  • cataracts
  • uveitis

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Published Papers (4 papers)

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Research

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20 pages, 2552 KB  
Article
Impact of Orchiectomy on Oxidative Stress-Induced Neurodegeneration in the Male Rat Retina: A Proteomic Analysis
by Khadiza Zaman, Ammar Kapic, Vien Nguyen and Katalin Prokai-Tatrai
Antioxidants 2026, 15(4), 479; https://doi.org/10.3390/antiox15040479 - 12 Apr 2026
Viewed by 739
Abstract
Elevated oxidative stress (OS) is a primary driver of ocular neurodegeneration, worsening with age-related declines in gonadal hormones. While the loss of endogenous 17β-estradiol (E2) is a recognized risk factor for retinal degeneration in females, the impact of testosterone depletion in males remains [...] Read more.
Elevated oxidative stress (OS) is a primary driver of ocular neurodegeneration, worsening with age-related declines in gonadal hormones. While the loss of endogenous 17β-estradiol (E2) is a recognized risk factor for retinal degeneration in females, the impact of testosterone depletion in males remains poorly understood. To address this knowledge gap, we employed mass spectrometry-based proteomics and bioinformatic pipelines to characterize retinal protein shifts triggered by orchiectomy (ORX) in the Brown Norway rat. Proteins from ORX and intact retinas were analyzed via a discovery-driven approach using nanoflow liquid chromatography–tandem mass spectrometry with data-independent acquisition. Ingenuity Pathway Analysis® of differentially expressed proteins (DEPs) revealed nearly 300 significantly regulated canonical pathways, many associated with OS, free radical detoxification, mitochondrial dysfunction and ophthalmic disease. A selected panel of DEPs was verified by protein-targeted data extraction. Notably, pathway analysis revealed the prominence of estrogen receptor signaling over androgen receptor signaling in the retina, despite the loss of male sex hormones following ORX. These findings indicate that E2-mediated pathways play a more significant role in male retinal protection than previously recognized. Our study provides the first proteomics-based evidence of the male rat retina’s heightened susceptibility to ORX-associated OS, identifying potential targets for treating sex hormone deprivation-associated retinal neurodegeneration. Full article
(This article belongs to the Special Issue Role of Oxidative Stress in Eye Diseases)
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22 pages, 4654 KB  
Article
PM10 Disrupts Mitochondrial Homeostasis in Corneal Epithelial Cells: Protective Effects of SKQ1
by Mallika Somayajulu, Robert Wright, Farooq S. Muhammed, Sharon A. McClellan, Ahmed S. Ibrahim and Linda D. Hazlett
Antioxidants 2026, 15(3), 284; https://doi.org/10.3390/antiox15030284 - 25 Feb 2026
Viewed by 681
Abstract
Airborne particulate matter with a diameter of <10 μm (PM10) can damage the corneal epithelium by inducing oxidative stress, disrupting the NRF2 antioxidant pathway, and triggering epithelial barrier dysfunction and inflammation. However, the role of mitochondria in mediating PM10-induced [...] Read more.
Airborne particulate matter with a diameter of <10 μm (PM10) can damage the corneal epithelium by inducing oxidative stress, disrupting the NRF2 antioxidant pathway, and triggering epithelial barrier dysfunction and inflammation. However, the role of mitochondria in mediating PM10-induced damage remains unexplored. This study investigated the impact of PM10 on mitochondrial homeostasis in both immortalized human corneal epithelial cells (HCE-2) and the mouse corneal epithelium, as well as the protective effects of SKQ1. For in vivo assessment, female C57BL/6 mice were exposed to either control air or PM10 (±SKQ1) in a whole-body exposure chamber for 2 weeks (3 h/day, 5 days/week, with weekends off). In vitro, HCE-2 cells were exposed to 100 μg/mL PM10 (±SKQ1) for 24 h, and mitochondrial function and morphology were evaluated. In vitro, PM10 significantly impaired mitochondrial function by reducing basal, maximal, and ATP-linked respiration; reserve capacity; and coupling efficiency compared to the control and SKQ1 groups. PM10 also downregulated mitofusin1 (MFN1) and optic atrophy1 (OPA1) and upregulated dynamin-related protein1 (DRP1) and mitochondrial fission protein1 (FIS1) in HCE-2 cells. In addition, PM10 exposure significantly decreased the mitochondrial membrane potential; mitochondrial DNA copy number; and cytochrome c oxidase subunit 4 isoform 1 (COX4i1), mitochondrial transcription factor A (TFAM), and peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1α) levels. SKQ1 pre-treatment significantly attenuated these effects. In vivo, PM10 exposure significantly decreased the levels of MFN1, TFAM, COX4i1, and superoxide dismutase (SOD2), whereas SKQ1 treatment significantly reversed these effects. Overall, these findings demonstrate that PM10 exposure induces mitochondrial fragmentation, disrupts mitochondrial biogenesis and quality control, and reduces mitochondrial respiration, resulting in mitochondrial dysfunction. SKQ1 effectively reversed these changes, suggesting its potential as a therapeutic strategy to protect corneal epithelial cells from PM10-induced mitochondrial damage. Full article
(This article belongs to the Special Issue Role of Oxidative Stress in Eye Diseases)
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20 pages, 2042 KB  
Article
Effect of 3′,4′-Dihydroxyflavonol Eye Drops in a Rat Model of Dispase-Induced Proliferative Vitreoretinopathy
by Elsa C. Chan, Cheng Zeng, Chi D. Luu, Carla J. Abbott, Nicholas T. Chan, Keshava K. Datta, Nicholas Williamson, Penelope J. Allen and Jennifer C. Fan Gaskin
Antioxidants 2025, 14(12), 1414; https://doi.org/10.3390/antiox14121414 - 27 Nov 2025
Viewed by 881
Abstract
(1) Background: Proliferative vitreoretinopathy (PVR) is the most common cause of failure in retinal detachment surgery and often leads to blindness. Oxidative stress is known to contribute to scar formation; therefore, reducing oxidative stress may protect against PVR development. This study investigated the [...] Read more.
(1) Background: Proliferative vitreoretinopathy (PVR) is the most common cause of failure in retinal detachment surgery and often leads to blindness. Oxidative stress is known to contribute to scar formation; therefore, reducing oxidative stress may protect against PVR development. This study investigated the therapeutic effects of the antioxidant 3′,4′-dihydroxyflavonol (DiOHF) in two preclinical models of PVR. (2) Methods: A retinal pigment epithelial cell line (ARPE-19) was used to investigate the anti-fibrotic effects of DiOHF. PVR was induced in one eye of each animal using dispase. Animals then received either vehicle or DiOHF eye drops in both eyes for 28 days. Eyes were harvested for mass spectrometry to perform proteomic analysis or to quantify tissue accumulation of DiOHF. Proteomic analysis was also performed in ARPE to validate these findings. (3) Results: In DiOHF-treated eyes with induced PVR, proteomic profiles showed reduced fibrosis, inflammation, cell migration, and oxidative stress compared with vehicle-treated PVR eyes. The in vitro studies confirmed that DiOHF inhibited wound healing responses, cell contraction, proliferation, and the generation of reactive oxygen species in ARPE-19 cells. Proteomic analysis in ARPE-19 also showed a similar trend. (4) Conclusions: This study provides compelling evidence that DiOHF eye drops offer protective effects against PVR in preclinical models. Full article
(This article belongs to the Special Issue Role of Oxidative Stress in Eye Diseases)
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Review

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26 pages, 2013 KB  
Review
Title Oxidative Stress in Age-Related Macular Degeneration: From Molecular Mechanisms to Emerging Therapeutic Targets
by Tatsuya Mimura and Hidetaka Noma
Antioxidants 2025, 14(10), 1251; https://doi.org/10.3390/antiox14101251 - 18 Oct 2025
Cited by 6 | Viewed by 3235
Abstract
Age-related macular degeneration (AMD) is a leading cause of irreversible visual impairment in the elderly, and oxidative stress, primarily mediated by reactive oxygen species (ROS), is widely recognized as a central driver of its onset and progression. The retina is highly susceptible to [...] Read more.
Age-related macular degeneration (AMD) is a leading cause of irreversible visual impairment in the elderly, and oxidative stress, primarily mediated by reactive oxygen species (ROS), is widely recognized as a central driver of its onset and progression. The retina is highly susceptible to oxidative damage due to its elevated oxygen consumption, abundant polyunsaturated fatty acids, and continuous exposure to light. Recent studies have elucidated molecular mechanisms in which mitochondrial dysfunction, disruption of redox homeostasis, inflammation, and complement activation interact to promote degeneration of retinal pigment epithelium (RPE) and photoreceptor cells. In addition to age-related oxidative stress, environmental factors such as motor vehicle exhaust and volatile organic compounds (VOCs) can accelerate the accumulation of lipofuscin and drusen, thereby fostering a chronic pro-inflammatory milieu. From a therapeutic perspective, beyond conventional antioxidant supplementation, emerging strategies targeting oxidative stress-related pathways have gained attention, including mitochondrial protectants, activation of the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway, anti-inflammatory agents, and gene therapy. Importantly, several innovative approaches are under investigation, such as saffron supplementation with neuroprotective properties, drug repositioning of levodopa, and nanotechnology-based delivery systems to enhance retinal bioavailability of antioxidants and gene therapies. This review summarizes the pathophysiological role of oxidative stress in AMD from a molecular mechanistic perspective and discusses recent advances in research and novel therapeutic targets. Full article
(This article belongs to the Special Issue Role of Oxidative Stress in Eye Diseases)
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