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Molecular Mechanisms of Retinal Degeneration and How to Avoid It—2nd Edition

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 20 January 2025 | Viewed by 9346

Special Issue Editors

Prof. Dr. Tamás Kovács-Öller

E-Mail Website
Guest Editor
Szentagothai Research Centre, University of Pécs, 7624 Pécs, Hungary
Interests: gap junction; retina; neurobiology; patch clamp; calcium-imaging; vision
Special Issues, Collections and Topics in MDPI journals
Dr. Bela Volgyi

E-Mail Website
Guest Editor
Retinal Neurobiology Rresearch Group, Pécsi Tudományegyetem, 7622 Pecs, Hungary
Interests: vision; retinal signal processing; ganglion cells; population coding; electrical synapses; parallel signaling; morphological/functional classification
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Vision is the most important sensory modality in vertebrates in general and as such, it is the most feared sense to lose. The retina is the site for visual perception and we desperately need new tools and advanced therapeutic regimens to avoid retinal regeneration or at least slow down ongoing vision deteriorating diseases including glaucoma, diabetic retinopathy, age-related macular degeneration, myopia, retinal vascular disease, traumatic brain injuries, and many others.

Most cell types in the retina are involved in the deterioration process and thus suffer from these diseases including the neurons (ganglion cells, amacrine cells, bipolar cells, horizontal cells, and photoreceptors) as well non-neuronal (astrocytes, microglia, and Müller cells) cells. Comprehending the molecular mechanisms by which these diseases alter their function is crucial. Our special issue aims to widen our knowledge to help understand the disease phenotypes at all investigation levels since there is still a lack of information in identifying potential targets for regeneration or at least help retinal survival and restore vision.

We are looking forward to receiving your original research manuscripts or reviews.

Prof. Dr. Tamás Kovács-Öller
Dr. Bela Volgyi
Guest Editors

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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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
  • retina
  • disease
  • glaucoma
  • diabetic retinopathy
  • age-related macular degeneration
  • myopia
  • retinal vascular disease
  • traumatic brain injury
  • molecular mechanisms

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Published Papers (5 papers)

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Research

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24 pages, 1646 KiB  
Article
The Impact of ARMS2 (rs10490924), VEGFA (rs3024997), TNFRSF1B (rs1061622), TNFRSF1A (rs4149576), and IL1B1 (rs1143623) Polymorphisms and Serum Levels on Age-Related Macular Degeneration Development and Therapeutic Responses
by Dzastina Cebatoriene, Alvita Vilkeviciute, Greta Gedvilaite-Vaicechauskiene, Monika Duseikaite, Akvile Bruzaite, Loresa Kriauciuniene, Dalia Zaliuniene and Rasa Liutkeviciene
Int. J. Mol. Sci. 2024, 25(17), 9750; https://doi.org/10.3390/ijms25179750 - 9 Sep 2024
Viewed by 831
Abstract
Age-related macular degeneration (AMD) is a major global health problem as it is the leading cause of irreversible loss of central vision in the aging population. Anti-vascular endothelial growth factor (anti-VEGF) therapies are effective but do not respond optimally in all patients. This [...] Read more.
Age-related macular degeneration (AMD) is a major global health problem as it is the leading cause of irreversible loss of central vision in the aging population. Anti-vascular endothelial growth factor (anti-VEGF) therapies are effective but do not respond optimally in all patients. This study investigates the genetic factors associated with susceptibility to AMD and response to treatment, focusing on key polymorphisms in the ARMS2 (rs10490924), IL1B1 (rs1143623), TNFRSF1B (rs1061622), TNFRSF1A (rs4149576), VEGFA (rs3024997), ARMS2, IL1B1, TNFRSF1B, TNFRSF1A, and VEGFA serum levels in AMD development and treatment efficacy. This study examined the associations of specific genetic polymorphisms and serum protein levels with exudative and early AMD and the response to anti-VEGF treatment. The AA genotype of VEGFA (rs3024997) was significantly associated with a 20-fold reduction in the odds of exudative AMD compared to the GG + GA genotypes. Conversely, the TT genotype of ARMS2 (rs10490924) was linked to a 4.2-fold increase in the odds of exudative AMD compared to GG + GT genotypes. In females, each T allele of ARMS2 increased the odds by 2.3-fold, while in males, the TT genotype was associated with a 5-fold increase. Lower serum IL1B levels were observed in the exudative AMD group compared to the controls. Early AMD patients had higher serum TNFRSF1B levels than controls, particularly those with the GG genotype of TNFRSF1B rs1061622. Exudative AMD patients with the CC genotype of TNFRSF1A rs4149576 had lower serum TNFRSF1A levels compared to the controls. Visual acuity (VA) analysis showed that non-responders had better baseline VA than responders but experienced decreased VA after treatment, whereas responders showed improvement. Central retinal thickness (CRT) reduced significantly in responders after treatment and was lower in responders compared to non-responders after treatment. The T allele of TNFRSF1B rs1061622 was associated with a better response to anti-VEGF treatment under both dominant and additive genetic models. These findings highlight significant genetic and biochemical markers associated with AMD and treatment response. This study found that the VEGFA rs3024997 AA genotype reduces the odds of exudative AMD, while the ARMS2 rs10490924 TT genotype increases it. Lower serum IL1B levels and variations in TNFRSF1B and TNFRSF1A levels were linked to AMD. The TNFRSF1B rs1061622 T allele was associated with better anti-VEGF treatment response. These markers could potentially guide risk assessment and personalized treatment for AMD. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Retinal Degeneration and How to Avoid It—2nd Edition)
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21 pages, 4109 KiB  
Article
Effects of Fucoidans on Activated Retinal Microglia
by Philipp Dörschmann, Florentine Hunger, Hannah Schroth, Sibei Chen, Georg Kopplin, Johann Roider and Alexa Klettner
Int. J. Mol. Sci. 2024, 25(11), 6018; https://doi.org/10.3390/ijms25116018 - 30 May 2024
Viewed by 1027
Abstract
Sulfated marine polysaccharides, so-called fucoidans, have been shown to exhibit anti-inflammatory and immunomodulatory activities in retinal pigment epithelium (RPE). In this study, we tested the effects of different fucoidans (and of fucoidan-treated RPE cells) on retinal microglia to investigate whether its anti-inflammatory effect [...] Read more.
Sulfated marine polysaccharides, so-called fucoidans, have been shown to exhibit anti-inflammatory and immunomodulatory activities in retinal pigment epithelium (RPE). In this study, we tested the effects of different fucoidans (and of fucoidan-treated RPE cells) on retinal microglia to investigate whether its anti-inflammatory effect can be extrapolated to the innate immune cells of the retina. In addition, we tested whether fucoidan treatment influenced the anti-inflammatory effect of RPE cells on retinal microglia. Three fucoidans were tested (FVs from Fucus vesiculosus, Fuc1 and FucBB04 from Laminaria hyperborea) as well as the supernatant of primary porcine RPE treated with fucoidans for their effects on inflammatory activated (using lipopolysaccharide, LPS) microglia cell line SIM-A9 and primary porcine retinal microglia. Cell viability was detected with a tetrazolium assay (MTT), and morphology by Coomassie staining. Secretion of tumor necrosis factor alpha (TNFα), interleukin 1 beta (IL1β) and interleukin 8 (IL8) was detected with ELISA, gene expression (NOS2 (Nitric oxide synthase 2), and CXCL8 (IL8)) with qPCR. Phagocytosis was detected with a fluorescence assay. FucBB04 and FVs slightly reduced the viability of SIM-A9 and primary microglia, respectively. Treatment with RPE supernatants increased the viability of LPS-treated primary microglia. FVs and FucBB04 reduced the size of LPS-activated primary microglia, indicating an anti-inflammatory phenotype. RPE supernatant reduced the size of LPS-activated SIM-A9 cells. Proinflammatory cytokine secretion and gene expression in SIM-A9, as well as primary microglia, were not significantly affected by fucoidans, but RPE supernatants reduced the secretion of LPS-induced proinflammatory cytokine secretion in SIM-A9 and primary microglia. The phagocytosis ability of primary microglia was reduced by FucBB04. In conclusion, fucoidans exhibited only modest effects on inflammatorily activated microglia by maintaining their cell size under stimulation, while the anti-inflammatory effect of RPE cells on microglia irrespective of fucoidan treatment could be confirmed, stressing the role of RPE in regulating innate immunity in the retina. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Retinal Degeneration and How to Avoid It—2nd Edition)
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Review

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28 pages, 2189 KiB  
Review
Understanding the Impact of Polyunsaturated Fatty Acids on Age-Related Macular Degeneration: A Review
by Maëlis Brito, Capucine Sorbier, Nathalie Mignet, Vincent Boudy, Gerrit Borchard and Gaëlle Vacher
Int. J. Mol. Sci. 2024, 25(7), 4099; https://doi.org/10.3390/ijms25074099 - 7 Apr 2024
Cited by 2 | Viewed by 2333
Abstract
Age-related Macular Degeneration (AMD) is a multifactorial ocular pathology that destroys the photoreceptors of the macula. Two forms are distinguished, dry and wet AMD, with different pathophysiological mechanisms. Although treatments were shown to be effective in wet AMD, they remain a heavy burden [...] Read more.
Age-related Macular Degeneration (AMD) is a multifactorial ocular pathology that destroys the photoreceptors of the macula. Two forms are distinguished, dry and wet AMD, with different pathophysiological mechanisms. Although treatments were shown to be effective in wet AMD, they remain a heavy burden for patients and caregivers, resulting in a lack of patient compliance. For dry AMD, no real effective treatment is available in Europe. It is, therefore, essential to look for new approaches. Recently, the use of long-chain and very long-chain polyunsaturated fatty acids was identified as an interesting new therapeutic alternative. Indeed, the levels of these fatty acids, core components of photoreceptors, are significantly decreased in AMD patients. To better understand this pathology and to evaluate the efficacy of various molecules, in vitro and in vivo models reproducing the mechanisms of both types of AMD were developed. This article reviews the anatomy and the physiological aging of the retina and summarizes the clinical aspects, pathophysiological mechanisms of AMD and potential treatment strategies. In vitro and in vivo models of AMD are also presented. Finally, this manuscript focuses on the application of omega-3 fatty acids for the prevention and treatment of both types of AMD. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Retinal Degeneration and How to Avoid It—2nd Edition)
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19 pages, 1854 KiB  
Review
The Role of Galectin-3 in Retinal Degeneration and Other Ocular Diseases: A Potential Novel Biomarker and Therapeutic Target
by Ziyi Zhou, Zhaochen Feng, Xiaojia Sun, Yusheng Wang and Guorui Dou
Int. J. Mol. Sci. 2023, 24(21), 15516; https://doi.org/10.3390/ijms242115516 - 24 Oct 2023
Cited by 2 | Viewed by 1963
Abstract
Galectin-3 is the most studied member of the Galectin family, with a large range of mediation in biological activities such as cell growth, proliferation, apoptosis, differentiation, cell adhesion, and tissue repair, as well as in pathological processes such as inflammation, tissue fibrosis, and [...] Read more.
Galectin-3 is the most studied member of the Galectin family, with a large range of mediation in biological activities such as cell growth, proliferation, apoptosis, differentiation, cell adhesion, and tissue repair, as well as in pathological processes such as inflammation, tissue fibrosis, and angiogenesis. As is known to all, inflammation, aberrant cell apoptosis, and neovascularization are the main pathophysiological processes in retinal degeneration and many ocular diseases. Therefore, the review aims to conclude the role of Gal3 in the retinal degeneration of various diseases as well as the occurrence and development of the diseases and discuss its molecular mechanisms according to research in systemic diseases. At the same time, we summarized the predictive role of Gal3 as a biomarker and the clinical application of its inhibitors to discuss the possibility of Gal3 as a novel target for the treatment of ocular diseases. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Retinal Degeneration and How to Avoid It—2nd Edition)
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17 pages, 1069 KiB  
Review
Neurovascular Cell Death and Therapeutic Strategies for Diabetic Retinopathy
by Toshiyuki Oshitari
Int. J. Mol. Sci. 2023, 24(16), 12919; https://doi.org/10.3390/ijms241612919 - 18 Aug 2023
Cited by 9 | Viewed by 2394
Abstract
Diabetic retinopathy (DR) is a major complication of diabetes and a leading cause of blindness worldwide. DR was recently defined as a neurovascular disease associated with tissue-specific neurovascular impairment of the retina in patients with diabetes. Neurovascular cell death is the main cause [...] Read more.
Diabetic retinopathy (DR) is a major complication of diabetes and a leading cause of blindness worldwide. DR was recently defined as a neurovascular disease associated with tissue-specific neurovascular impairment of the retina in patients with diabetes. Neurovascular cell death is the main cause of neurovascular impairment in DR. Thus, neurovascular cell protection is a potential therapy for preventing the progression of DR. Growing evidence indicates that a variety of cell death pathways, such as apoptosis, necroptosis, ferroptosis, and pyroptosis, are associated with neurovascular cell death in DR. These forms of regulated cell death may serve as therapeutic targets for ameliorating the pathogenesis of DR. This review focuses on these cell death mechanisms and describes potential therapies for the treatment of DR that protect against neurovascular cell death. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Retinal Degeneration and How to Avoid It—2nd Edition)
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