Oxidative Stress in Diabetic Retinopathy and Other Retinal Diseases

A Special Issue of Antioxidants (ISSN 2076-3921) belonging to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: 28 February 2027 | Viewed by 1557

Editor


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Guest Editor
Department of Molecular and Cellular Biochemistry, Kangwon National University School of Medicine, Chuncheon 24341, Republic of Korea
Interests: diabetic microvascular complications; vascular dysfunction; diabetic retinopathy; age-related macular degeneration

Special Issue Information

Dear Colleagues,

Oxidative stress is a central mechanism underlying the pathogenesis of multiple retinal disorders and contributes significantly to progressive vision loss, including diabetic retinopathy, age-related macular degeneration, retinal vein occlusion, and optic neuropathy. The retina is particularly susceptible to oxidative damage because of its high metabolic activity, abundant polyunsaturated fatty acids, and continuous exposure to light. In diabetic retinopathy, which progresses from early non-proliferative to advanced proliferative stages, chronic hyperglycemia triggers excessive production of reactive oxygen species. This overproduction leads to mitochondrial dysfunction, vascular leakage, neuroinflammation, and disruption of the blood–retinal barrier. Similarly, oxidative stress plays a pivotal role in retinal pigment epithelial dysfunction, photoreceptor degeneration, and pathological neovascularization in age-related macular degeneration and other retinal diseases.

This Special Issue aims to highlight recent advances in elucidating the molecular mechanisms linking oxidative stress to retinal neurovascular injury and to explore emerging therapeutic strategies. We welcome original research articles and comprehensive reviews addressing redox signaling, mitochondrial dynamics, vascular and neuronal dysfunction, and innovative therapeutic interventions. Studies employing experimental animal models, translational research approaches, and well-designed clinical investigations are particularly encouraged.

By integrating fundamental mechanistic insights with clinical perspectives, this Special Issue seeks to promote the development of targeted strategies to prevent or slow the progression of retinal diseases and ultimately preserve visual function.

Prof. Dr. Kwon-Soo Ha
Guest Editor

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Keywords

  • vascular dysfunction
  • oxidative stress
  • mitochondrial dynamics
  • neurovascular dysfunction
  • diabetic retinopathy
  • age-related macular degeneration
  • retinal vein occlusion

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Published Papers (1 paper)

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Research

20 pages, 29652 KB  
Article
Biopolymer-Conjugated Human C-Peptide Provides Sustained Neuroprotection and Preserves Axonal Transport in a Mouse Model of NMDA-Induced Retinal Degeneration via Antioxidative Mechanisms
by Ji-Seok Yoon, Chan-Hee Moon, Tae-Yong Koh, Woo Ri Cho, Juha Lee, Minsoo Kim and Kwon-Soo Ha
Antioxidants 2026, 15(7), 911; https://doi.org/10.3390/antiox15070911 - 22 Jul 2026
Viewed by 1061
Abstract
Glutamate excitotoxicity is a key contributor to the pathogenesis of glaucoma, a leading cause of irreversible blindness worldwide; however, the molecular events driving progressive retinal ganglion cell (RGC) loss and axonal degeneration remain incompletely understood, and effective neuroprotective therapies are lacking. Here, we [...] Read more.
Glutamate excitotoxicity is a key contributor to the pathogenesis of glaucoma, a leading cause of irreversible blindness worldwide; however, the molecular events driving progressive retinal ganglion cell (RGC) loss and axonal degeneration remain incompletely understood, and effective neuroprotective therapies are lacking. Here, we evaluated the preventive potential of K9-C-peptide, a biopolymer-conjugated human C-peptide, in a mouse model of N-methyl-D-aspartate (NMDA)-induced retinal neurodegeneration and optic nerve axonal transport impairment, and examined potential mechanisms underlying its protective effects. In NMDA-induced excitotoxic mouse retinas, intracellular Ca2+ elevation mediated NMDA-induced oxidative stress, including both intracellular and mitochondrial reactive oxygen species (ROS) generation and lipid peroxidation. NMDA exposure induced activation of Müller glia and microglia and upregulation of inflammatory cytokines, ultimately leading to RGC death; these effects were attenuated by prolonged intraocular delivery of ROS scavengers. K9-C-peptide significantly reduced NMDA-induced retinal degeneration, including RGC loss and retinal thinning, and preserved optic nerve axonal transport function in both whole-mount retinas and optic nerve longitudinal sections. These protective effects were associated with suppression of NMDA-induced oxidative stress, mitochondrial dysfunction, and inflammation and reactive gliosis, without altering intracellular Ca2+ levels. Notably, sustained intraocular delivery of human C-peptide conferred robust neuroprotection for at least 3 weeks against NMDA-induced retinal degeneration and optic nerve axonal transport impairment. These findings suggest that K9-C-peptide acts as a long-acting neuroprotective agent that mitigates oxidative stress-driven retinal damage and axonal dysfunction, highlighting its translational potential as a C-peptide-based neuroprotective strategy for retinal glutamate excitotoxicity. Full article
(This article belongs to the Special Issue Oxidative Stress in Diabetic Retinopathy and Other Retinal Diseases)
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