Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
8.8
7.0
Journals
Antioxidants
Special Issues
Oxidative Stress in the Retina Diseases
share announcement

Oxidative Stress in the Retina 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: closed (28 February 2022) | Viewed by 21727

Special Issue Editor

Dr. Isabel Pinilla

E-Mail Website
Guest Editor
1. Department of Ophthalmology, Lozano Blesa University Hospital, Zaragoza, Spain
2. Aragón Health Research Institute (IIS Aragón), Zaragoza, Spain
Interests: retinal degeneration; inherited retinal dystrophies; age-related macular degeneration; optical coherence tomography; retinal imaging

Special Issue Information

Dear Colleagues,

Oxidative stress, which represents an imbalance between the production and elimination of reactive oxygen species (ROS), plays an important role in the pathogenesis of many neurodegenerative diseases, including retinal conditions such as age-related macular degeneration (AMD), diabetic retinopathy, or inherited retinal dystrophies (IRD). Oxidative damage and inflammation are strongly connected in several eye diseases and have been shown in both in vitro and in vivo studies. The retina is exposed to high levels of oxidative stress that could be enhanced by age or pathologies. ROS are one of the main responsible mechanisms of the pathophysiology of retinal degeneration. The prevention of ROS formation and their damage will be an important target for treating these diseases or avoiding their appearance or progression.

A good knowledge of the mechanism implicated in ROS generation is crucial. The antioxidant defenses of our organism and the importance of oxidative stress and mitochondrial DNA damage should be explored as the origin of photoreceptor and RPE loss.

In this Special Issue, we welcome submissions of original research, review articles, and clinical trial results related to any aspect of the role of oxidative stress, mitochondrial dysfunction, and inflammation in the pathogenesis of ocular diseases, mainly retinal degeneration, including AMD, IRD, and diabetic retinopathy, the identification of the damage, and therapeutic approaches.

Dr. Isabel Pinilla
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

  • Retinal degeneration
  • Oxidative damage
  • Reactive oxygen species
  • Inflammatory mediators
  • Mitochondrial dysfunction
  • Antioxidant therapy

Published Papers (7 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Editorial

Jump to: Research, Review

3 pages, 191 KiB  
Editorial
Oxidative Stress as a Main Contributor of Retinal Degenerative Diseases
by Isabel Pinilla and Victoria Maneu
Antioxidants 2022, 11(6), 1190; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox11061190 - 17 Jun 2022
Cited by 2 | Viewed by 1407
Abstract
Retinal degenerative diseases, including inherited retinal dystrophies (IRDs) and acquired multifactorial diseases, such as age-related macular degeneration (AMD), diabetic retinopathy (DR) or ganglion cell damage secondary to glaucoma or other pathologies, are the main causes of blindness in developed countries [...] Full article
(This article belongs to the Special Issue Oxidative Stress in the Retina Diseases)

Research

Jump to: Editorial, Review

18 pages, 2272 KiB  
Article
Effects of Resveratrol on Vascular Function in Retinal Ischemia-Reperfusion Injury
by Panagiotis Chronopoulos, Caroline Manicam, Jenia Kouchek Zadeh, Panagiotis Laspas, Johanna Charlotte Unkrig, Marie Luise Göbel, Aytan Musayeva, Norbert Pfeiffer, Matthias Oelze, Andreas Daiber, Huige Li, Ning Xia and Adrian Gericke
Antioxidants 2023, 12(4), 853; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox12040853 - 01 Apr 2023
Cited by 6 | Viewed by 1963
Abstract
Ischemia-reperfusion (I/R) events are involved in the development of various ocular pathologies, e.g., retinal artery or vein occlusion. We tested the hypothesis that resveratrol is protective against I/R injury in the murine retina. Intraocular pressure (IOP) was elevated in anaesthetized mice to 110 [...] Read more.
Ischemia-reperfusion (I/R) events are involved in the development of various ocular pathologies, e.g., retinal artery or vein occlusion. We tested the hypothesis that resveratrol is protective against I/R injury in the murine retina. Intraocular pressure (IOP) was elevated in anaesthetized mice to 110 mm Hg for 45 min via a micropipette placed in the anterior chamber to induce ocular ischemia. In the fellow eye, which served as control, IOP was kept at a physiological level. One group received resveratrol (30 mg/kg/day p.o. once daily) starting one day before the I/R event, whereas the other group of mice received vehicle solution only. On day eight after the I/R event, mice were sacrificed and retinal wholemounts were prepared and immuno-stained using a Brn3a antibody to quantify retinal ganglion cells. Reactivity of retinal arterioles was measured in retinal vascular preparations using video microscopy. Reactive oxygen species (ROS) and nitrogen species (RNS) were quantified in ocular cryosections by dihydroethidium and anti-3-nitrotyrosine staining, respectively. Moreover, hypoxic, redox and nitric oxide synthase gene expression was quantified in retinal explants by PCR. I/R significantly diminished retinal ganglion cell number in vehicle-treated mice. Conversely, only a negligible reduction in retinal ganglion cell number was observed in resveratrol-treated mice following I/R. Endothelial function and autoregulation were markedly reduced, which was accompanied by increased ROS and RNS in retinal blood vessels of vehicle-exposed mice following I/R, whereas resveratrol preserved vascular endothelial function and autoregulation and blunted ROS and RNS formation. Moreover, resveratrol reduced I/R-induced mRNA expression for the prooxidant enzyme, nicotinamide adenine dinucleotide phosphate oxidase 2 (NOX2). Our data provide evidence that resveratrol protects from I/R-induced retinal ganglion cell loss and endothelial dysfunction in the murine retina by reducing nitro-oxidative stress possibly via suppression of NOX2 upregulation. Full article
(This article belongs to the Special Issue Oxidative Stress in the Retina Diseases)
►▼ Show Figures

Figure 1

16 pages, 8156 KiB  
Article
Overexpression of CERKL Protects Retinal Pigment Epithelium Mitochondria from Oxidative Stress Effects
by Rocío García-Arroyo, Aleix Gavaldà-Navarro, Francesc Villarroya, Gemma Marfany and Serena Mirra
Antioxidants 2021, 10(12), 2018; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10122018 - 19 Dec 2021
Cited by 7 | Viewed by 3695
Abstract
The precise function of CERKL, a Retinitis Pigmentosa (RP) causative gene, is not yet fully understood. There is evidence that CERKL is involved in the regulation of autophagy, stress granules, and mitochondrial metabolism, and it is considered a gene that is resilient [...] Read more.
The precise function of CERKL, a Retinitis Pigmentosa (RP) causative gene, is not yet fully understood. There is evidence that CERKL is involved in the regulation of autophagy, stress granules, and mitochondrial metabolism, and it is considered a gene that is resilient against oxidative stress in the retina. Mutations in most RP genes affect photoreceptors, but retinal pigment epithelium (RPE) cells may be also altered. Here, we aimed to analyze the effect of CERKL overexpression and depletion in vivo and in vitro, focusing on the state of the mitochondrial network under oxidative stress conditions. Our work indicates that the depletion of CERKL increases the vulnerability of RPE mitochondria, which show a shorter size and altered shape, particularly upon sodium arsenite treatment. CERKL-depleted cells have dysfunctional mitochondrial respiration particularly upon oxidative stress conditions. The overexpression of two human CERKL isoforms (558 aa and 419 aa), which display different protein domains, shows that a pool of CERKL localizes at mitochondria in RPE cells and that CERKL protects the mitochondrial network—both in size and shape—against oxidative stress. Our results support CERKL being a resilient gene that regulates the mitochondrial network in RPE as in retinal neurons and suggest that RPE cell alteration contributes to particular phenotypic traits in patients carrying CERKL mutations. Full article
(This article belongs to the Special Issue Oxidative Stress in the Retina Diseases)
►▼ Show Figures

Figure 1

16 pages, 1749 KiB  
Article
Effects of Daily Melatonin Supplementation on Visual Loss, Circadian Rhythms, and Hepatic Oxidative Damage in a Rodent Model of Retinitis Pigmentosa
by Lorena Fuentes-Broto, Lorena Perdices, Francisco Segura, Elvira Orduna-Hospital, Gema Insa-Sánchez, Ana I. Sánchez-Cano, Nicolás Cuenca and Isabel Pinilla
Antioxidants 2021, 10(11), 1853; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10111853 - 22 Nov 2021
Cited by 4 | Viewed by 3012
Abstract
Retinitis pigmentosa (RP) is a group of inherited neurodegenerative diseases characterized by a progressive loss of visual function that primarily affect photoreceptors, resulting in the complete disorganization and remodeling of the retina. Progression of the disease is enhanced by increased oxidative stress in [...] Read more.
Retinitis pigmentosa (RP) is a group of inherited neurodegenerative diseases characterized by a progressive loss of visual function that primarily affect photoreceptors, resulting in the complete disorganization and remodeling of the retina. Progression of the disease is enhanced by increased oxidative stress in the retina, aqueous humor, plasma, and liver of RP animal models and patients. Melatonin has beneficial effects against age-related macular degeneration, glaucoma, and diabetic retinopathy, in which oxidative stress plays a key role. In the present study, we used the P23HxLE rat as an animal model of RP. Melatonin treatment (10 mg/kg b.w. daily in drinking water for 6 months) improved the parameters of visual function and decreased the rate of desynchronization of the circadian rhythm, both in P23HxLE and wild-type rats. Melatonin reduced oxidative stress and increased antioxidant defenses in P23HxLE animals. In wild-type animals, melatonin did not modify any of the oxidative stress markers analyzed and reduced the levels of total antioxidant defenses. Treatment with melatonin improved visual function, circadian synchronization, and hepatic oxidative stress in P23HxLE rats, an RP model, and had beneficial effects against age-related visual damage in wild-type rats. Full article
(This article belongs to the Special Issue Oxidative Stress in the Retina Diseases)
►▼ Show Figures

Graphical abstract

16 pages, 3594 KiB  
Article
Quercetin Alleviates the Accumulation of Superoxide in Sodium Iodate-Induced Retinal Autophagy by Regulating Mitochondrial Reactive Oxygen Species Homeostasis through Enhanced Deacetyl-SOD2 via the Nrf2-PGC-1α-Sirt1 Pathway
by Min-Yen Hsu, Yai-Ping Hsiao, Yu-Ta Lin, Connie Chen, Chee-Ming Lee, Wen-Chieh Liao, Shang-Chun Tsou, Hui-Wen Lin and Yuan-Yen Chang
Antioxidants 2021, 10(7), 1125; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10071125 - 14 Jul 2021
Cited by 23 | Viewed by 4074
Abstract
Oxidative damage of retinal pigment epithelium (RPE) cells plays an important role in the pathogenesis of blindness-related diseases, such as age-related macular degeneration (AMD). Quercetin, a bioactive flavonoid compound, has been shown to have a protective effect against oxidative stress-induced cell apoptosis and [...] Read more.
Oxidative damage of retinal pigment epithelium (RPE) cells plays an important role in the pathogenesis of blindness-related diseases, such as age-related macular degeneration (AMD). Quercetin, a bioactive flavonoid compound, has been shown to have a protective effect against oxidative stress-induced cell apoptosis and inflammation in RPE cells; however, the detailed mechanism underlying this protective effect is unclear. Therefore, the aim of this study was to investigate the regulatory mechanism of quercetin in a sodium iodate (NaIO3)-induced retinal damage. The clinical features of the mice, the production of oxidative stress, and the activity of autophagy and mitochondrial biogenesis were examined. In the mouse model, NaIO3 treatment caused changes in the retinal structure and reduced pupil constriction, and quercetin treatment reversed the oxidative stress-related pathology by decreasing the level of superoxide dismutase 2 (SOD2) while enhancing the serum levels of catalase and glutathione. The increased level of reactive oxygen species in the NaIO3-treated ARPE19 cells was improved by treatment with quercetin, accompanied by a reduction in autophagy and mitochondrial biogenesis. Our findings indicated that the effects of quercetin on regulating the generation of mtROS were dependent on increased levels of deacetyl-SOD2 through the Nrf2-PGC-1α-Sirt1 signaling pathway. These results demonstrated that quercetin may have potential therapeutic efficacy for the treatment of AMD through the regulation of mtROS homeostasis. Full article
(This article belongs to the Special Issue Oxidative Stress in the Retina Diseases)
►▼ Show Figures

Figure 1

19 pages, 3192 KiB  
Article
Spinach Methanolic Extract Attenuates the Retinal Degeneration in Diabetic Rats
by Rocio Bautista-Pérez, Agustina Cano-Martínez, Elisa Gutiérrez-Velázquez, Martín Martínez-Rosas, Rosa M. Pérez-Gutiérrez, Francisco Jiménez-Gómez and Javier Flores-Estrada
Antioxidants 2021, 10(5), 717; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10050717 - 03 May 2021
Cited by 7 | Viewed by 2664
Abstract
It has been suggested that spinach methanolic extract (SME) inhibits the formation of advanced glycation end products (AGEs), which are increased during diabetes progression, so it is important to know if SME has beneficial effects in the diabetic retina. In this study, in [...] Read more.
It has been suggested that spinach methanolic extract (SME) inhibits the formation of advanced glycation end products (AGEs), which are increased during diabetes progression, so it is important to know if SME has beneficial effects in the diabetic retina. In this study, in vitro assays showed that SME inhibits glycation, carbonyl groups formation, and reduced-thiol groups depletion in bovine serum albumin incubated either reducing sugars or methylglyoxal. The SME effect in retinas of streptozotocin-induced diabetic rats (STZ) was also studied (n = 10) in the normoglycemic group, STZ, STZ rats treated with SME, and STZ rats treated with aminoguanidine (anti-AGEs reference group) during 12 weeks. The retina was sectioned and immunostained for Nε-carboxymethyl lysine (CML), receptor RAGE, NADPH-Nox4, inducible nitric oxide synthase (iNOS), 3-nitrotyrosine (NT), nuclear NF-κB, vascular endothelial growth factor (VEGF), glial fibrillary acidic protein (GFAP), S100B protein, and TUNEL assay. Lipid peroxidation was determined in the whole retina by malondialdehyde (MDA) levels. The results showed that in the diabetic retina, SME reduced the CML-RAGE co-localization, oxidative stress (NOX4, iNOS, NT, MDA), inflammation (NF-κB, VEGF, S100B, GFAP), and apoptosis (p < 0.05). Therefore, SME could attenuate the retinal degeneration by inhibition of CML–RAGE interaction. Full article
(This article belongs to the Special Issue Oxidative Stress in the Retina Diseases)
►▼ Show Figures

Figure 1

Review

Jump to: Editorial, Research

55 pages, 795 KiB  
Review
Inherited Retinal Dystrophies: Role of Oxidative Stress and Inflammation in Their Physiopathology and Therapeutic Implications
by Isabel Pinilla, Victoria Maneu, Laura Campello, Laura Fernández-Sánchez, Natalia Martínez-Gil, Oksana Kutsyr, Xavier Sánchez-Sáez, Carla Sánchez-Castillo, Pedro Lax and Nicolás Cuenca
Antioxidants 2022, 11(6), 1086; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox11061086 - 30 May 2022
Cited by 18 | Viewed by 3949
Abstract
Inherited retinal dystrophies (IRDs) are a large group of genetically and clinically heterogeneous diseases characterized by the progressive degeneration of the retina, ultimately leading to loss of visual function. Oxidative stress and inflammation play fundamental roles in the physiopathology of these diseases. Photoreceptor [...] Read more.
Inherited retinal dystrophies (IRDs) are a large group of genetically and clinically heterogeneous diseases characterized by the progressive degeneration of the retina, ultimately leading to loss of visual function. Oxidative stress and inflammation play fundamental roles in the physiopathology of these diseases. Photoreceptor cell death induces an inflammatory state in the retina. The activation of several molecular pathways triggers different cellular responses to injury, including the activation of microglia to eliminate debris and recruit inflammatory cells from circulation. Therapeutical options for IRDs are currently limited, although a small number of patients have been successfully treated by gene therapy. Many other therapeutic strategies are being pursued to mitigate the deleterious effects of IRDs associated with oxidative metabolism and/or inflammation, including inhibiting reactive oxygen species’ accumulation and inflammatory responses, and blocking autophagy. Several compounds are being tested in clinical trials, generating great expectations for their implementation. The present review discusses the main death mechanisms that occur in IRDs and the latest therapies that are under investigation. Full article
(This article belongs to the Special Issue Oxidative Stress in the Retina Diseases)
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-7
Back to TopTop