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14.7
8.2
Journals
Antioxidants
Special Issues
Antioxidant Defenses and Inflammation in Diabetic Retinopathy
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Antioxidant Defenses and Inflammation in Diabetic Retinopathy

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 November 2026 | Viewed by 499

Editor

Dr. Devy Deliyanti

E-Mail Website
Guest Editor
Department of Anatomy and Physiology, School of Biomedical Sciences, University of Melbourne, Parkville, VIC 3010, Australia
Interests: diabetic retinopathy; retinal inflammation; regulatory T cells; oxidative stress; immunotherapy; B cells

Special Issue Information

Dear Colleagues,

Diabetic retinopathy is a severe microvascular complication of diabetes and the leading cause of blindness in working-age adults. Oxidative stress and inflammation are key pathological events that contribute to the development of diabetic retinopathy. The retina, with its high oxygen consumption and high level of polyunsaturated fatty acids, is particularly susceptible to oxidative stress, which can lead to retinal cell death and dysfunction.

The body’s natural antioxidant defenses play a crucial role in protecting the retina from this damage. However, in diabetic retinopathy, these systems are often compromised, leading to an imbalance between pro-oxidants and antioxidants. This oxidative imbalance triggers a cascade of inflammatory responses, including the activation of various immune cells and the production of pro-inflammatory cytokines, further exacerbating retinal injury.

This Special Issue aims to bring together the latest research on antioxidant defenses and inflammation in diabetic retinopathy. We invite the submission of original research and review articles exploring the mechanisms of oxidative stress and ocular/systemic inflammation, and the role of specific antioxidants and enzymes. We also welcome submissions on novel therapeutic strategies targeting these pathways to treat or prevent diabetic retinopathy. We look forward to your contributions.

Dr. Devy Deliyanti
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-anonymized 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

  • retinal injury
  • diabetic retinopathy
  • retinal inflammation
  • cell death
  • antioxidant
  • pro-oxidants
  • oxidative stress

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Published Papers (1 paper)

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Research

25 pages, 6634 KB  
Article
TSPO Modulation by PIGA-1138 Attenuates Oxidative Stress and Preserves Retinal Function in Experimental Diabetic Retinopathy
by Alessia Galante, Francesca Corsi, Rosario Amato, Sabrina Taliani, Federico Da Settimo, Maurizio Cammalleri, Ilaria Piano, Massimo Dal Monte and Claudia Gargini
Antioxidants 2026, 15(8), 1000; https://doi.org/10.3390/antiox15081000 - 12 Aug 2026
Viewed by 106
Abstract
Introduction: Diabetic retinopathy (DR) is characterized by early retinal neurodegeneration accompanied by progressive alterations of the retinal microvasculature, both exacerbated by hyperglycemia-induced oxidative stress and inflammation. Mitochondrial dysfunction critically contributes to neuronal loss and vascular impairment. The 18 kDa Translocator Protein (TSPO) is [...] Read more.
Introduction: Diabetic retinopathy (DR) is characterized by early retinal neurodegeneration accompanied by progressive alterations of the retinal microvasculature, both exacerbated by hyperglycemia-induced oxidative stress and inflammation. Mitochondrial dysfunction critically contributes to neuronal loss and vascular impairment. The 18 kDa Translocator Protein (TSPO) is a mitochondrial outer membrane protein whose expression is increased in activated retinal glial cells and represents a promising target to modulate neuroinflammation and oxidative stress. This study evaluates the therapeutic potential of the TSPO ligand PIGA-1138 in experimental models of DR. Methods: PIGA-1138 (3 µM in vitro; 10 mg/kg/day, i.p., in vivo) was evaluated in high glucose (HG)-exposed 661W retinal cells and in streptozotocin (STZ, 150 mg/kg)-induced diabetic C57BL/6J mice. Cell viability, mitochondrial function, oxidative stress, and Nrf2, HO-1, and SOD1 expression were assessed in vitro. Retinal function and morphology were evaluated in vivo by electroretinography (ERG), visual acuity testing, and optical coherence tomography (OCT) at 30 and 60 days after diabetes induction. Results: PIGA-1138 significantly improved cell viability, reducing apoptosis (TUNEL p ≤ 0.01), preserving mitochondrial membrane potential (MitoRed p ≤ 0.01), reducing oxidative damage, and enhancing Nrf2 nuclear translocation together with HO-1 (p ≤ 0.05) and SOD1 (p ≤ 0.01) expression in HG-treated retinal cells. In diabetic mice, treatment preserved ERG responses and limited retinal thinning at 60 days (p ≤ 0.01), while showing a trend toward preserving visual acuity. Conclusions: Targeting mitochondrial TSPO with PIGA-1138 attenuates key hallmarks of DR by mitigating oxidative stress, suppressing neuroinflammation, and preserving retinal structure and function. These findings support TSPO as a potential disease-modifying target for DR. Full article
(This article belongs to the Special Issue Antioxidant Defenses and Inflammation in Diabetic Retinopathy)
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