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Antioxidants
Special Issues
Oxidative Stress-Related Mechanisms and Antioxidant Therapy in Diabetic Retinopathy
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Oxidative Stress-Related Mechanisms and Antioxidant Therapy 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: closed (31 October 2022) | Viewed by 5965

Special Issue Editor

Dr. Ángel Luis Ortega

E-Mail Website
Guest Editor
Department of Physiology, Faculty of Pharmacy, University of Valencia, Vicente Andrés Estellés Av. s/n, 46100 Burjassot, Spain
Interests: diabetic retinopathy; oxidative stress; inflammation; vascular dysfunction; natural antioxidants; exosomes; early biomarkers of diabetic retinopathy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Diabetic retinopathy is the main cause of preventable vision loss and blindness in working-age adults. The loss of strict homeostatic glycemic control suffered in diabetes triggers neural and vascular damage to the retina in a complex sequence of events in which oxidative stress is a key factor. Both the direct action of reactive oxygen species on cell biomolecules and that mediated by their ability to enhance inflammatory responses cause damage to the structure and function of the retina. In recent years, the therapeutic strategies for diabetic retinopathy have focused on delaying the progression of the pathology in advanced stages, although previous neural and vascular damages are irreversible. Furthermore, recent studies show different antioxidant therapies to be effective in inhibiting, preventing, or delaying the development and progression of diabetic retinopathy. A thorough understanding of the generation and effects of oxidative stress on the hyperglycemic retina is needed, and of the use of new cellular targets and innovative therapies to prevent the irreversible damages induced in diabetic retinopathy.

We invite authors to submit original research findings, clinical trials, or reviews to this Special Issue, which will bring together current advances regarding the role of oxidative stress in the pathophysiology of diabetic retinopathy and the role of intercellular communication, as well as research related to the identification of novel early diagnostic biomarkers, the use of new therapeutic cellular targets, and the exploration of antioxidant and anti-inflammatory therapies in preventing the development of diabetic retinopathy.

Dr. Ángel Luis Ortega
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 100 words) can be sent to the Editorial Office for announcement on this website.

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

  • diabetic retinopathy
  • antioxidants
  • natural products
  • epigenetic mechanisms
  • biomarkers
  • inflammation
  • vascular dysfunction

Published Papers (2 papers)

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Research

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13 pages, 2017 KiB  
Article
Mitochondrial Fragmentation in a High Homocysteine Environment in Diabetic Retinopathy
by Renu A. Kowluru and Ghulam Mohammad
Antioxidants 2022, 11(2), 365; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox11020365 - 11 Feb 2022
Cited by 10 | Viewed by 1797
Abstract
Diabetic patients routinely have elevated homocysteine levels, and due to increase in oxidative stress, hyperhomocysteinemia is associated with increased mitochondrial damage. Mitochondrial homeostasis is directly related to the balance between their fission and fusion, and in diabetes this balance is disturbed. The aim [...] Read more.
Diabetic patients routinely have elevated homocysteine levels, and due to increase in oxidative stress, hyperhomocysteinemia is associated with increased mitochondrial damage. Mitochondrial homeostasis is directly related to the balance between their fission and fusion, and in diabetes this balance is disturbed. The aim of this study was to investigate the role of homocysteine in mitochondrial fission in diabetic retinopathy. Human retinal endothelial cells, either untransfected or transfected with siRNA of a fission protein (dynamin-related protein 1, Drp1) and incubated in the presence of 100 μM homocysteine, were analyzed for mitochondrial fragmentation by live-cell microscopy and GTPase activity of Drp1. Protective nucleoids and mtDNA damage were evaluated by SYBR DNA stain and by transcripts of mtDNA-encoded ND6 and cytochrome b. The role of nitrosylation of Drp1 in homocysteine-mediated exacerbation of mitochondrial fragmentation was determined by supplementing incubation medium with nitric-oxide inhibitor. Homocysteine exacerbated glucose-induced Drp1 activation and its nitrosylation, mitochondrial fragmentation and cell apoptosis, and further decreased nucleoids and mtDNA transcription. Drp1-siRNA or nitric-oxide inhibitor prevented glucose- and homocysteine-induced mitochondrial fission, damage and cell apoptosis. Thus, elevated homocysteine in a hyperglycemic environment increases Drp1 activity via increasing its nitrosylation, and this further fragments the mitochondria and increases apoptosis, ultimately leading to the development of diabetic retinopathy. Full article
(This article belongs to the Special Issue Oxidative Stress-Related Mechanisms and Antioxidant Therapy in Diabetic Retinopathy)
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Review

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29 pages, 12872 KiB  
Review
Contribution of Müller Cells in the Diabetic Retinopathy Development: Focus on Oxidative Stress and Inflammation
by Raul Carpi-Santos, Ricardo A. de Melo Reis, Flávia Carvalho Alcantara Gomes and Karin C. Calaza
Antioxidants 2022, 11(4), 617; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox11040617 - 23 Mar 2022
Cited by 25 | Viewed by 3555
Abstract
Diabetic retinopathy is a neurovascular complication of diabetes and the main cause of vision loss in adults. Glial cells have a key role in maintenance of central nervous system homeostasis. In the retina, the predominant element is the Müller cell, a specialized cell [...] Read more.
Diabetic retinopathy is a neurovascular complication of diabetes and the main cause of vision loss in adults. Glial cells have a key role in maintenance of central nervous system homeostasis. In the retina, the predominant element is the Müller cell, a specialized cell with radial morphology that spans all retinal layers and influences the function of the entire retinal circuitry. Müller cells provide metabolic support, regulation of extracellular composition, synaptic activity control, structural organization of the blood–retina barrier, antioxidant activity, and trophic support, among other roles. Therefore, impairments of Müller actions lead to retinal malfunctions. Accordingly, increasing evidence indicates that Müller cells are affected in diabetic retinopathy and may contribute to the severity of the disease. Here, we will survey recently described alterations in Müller cell functions and cellular events that contribute to diabetic retinopathy, especially related to oxidative stress and inflammation. This review sheds light on Müller cells as potential therapeutic targets of this disease. Full article
(This article belongs to the Special Issue Oxidative Stress-Related Mechanisms and Antioxidant Therapy in Diabetic Retinopathy)
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