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Special Issue "Retinal Degenerative Diseases 2.0"

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: 30 November 2023 | Viewed by 8180

Special Issue Editors

1. Department of Ophthalmology, Optometry, Ears Nose and Throat, and Pathology, Faculty of Medicine, University of Murcia, 30120 Murcia, Spain
2. Biosanitary Research Institute of Murcia-Virgen de la Arrixaca (IMIB-Arrixaca), C/ Campo, 12, 30120 El Palmar, Murcia, Spain
Interests: retina; retinal degeneration; retinal diseases; retinal ganglion cells; eyes; photoreceptor cells; eye diseases; taurine; contact lenses; dry eye; myopia control; optometry
Special Issues, Collections and Topics in MDPI journals
Department of Ophthalmology, Optometry, Ears Nose and Throat, and Pathology, Faculty of Medicine, Instituto Murciano de Investigación Biosanitaria Virgen de la Arrixaca (IMIB-Virgen de la Arrixaca), University of Murcia, 30120 Murcia, Spain
Interests: retinitis pigmentosa; retinal remodeling; glaucoma; phototoxicity microglia; Müller cells; bone-marrow-derived stem cells; stem cells, neurotrophic factors: cones; retinal ganglion cells; melanopsin; contact lenses
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues, 

The retina is part of the central nervous system with unique advantages for studying neurodegeneration and neuroprotection. Because of its location within the eye, it is easily accessible for local small-dose therapies. In addition, the efficacy of the treatments can be evaluated in vivo using morphological (e.g., optical coherence tomography, OCT) and functional tests (e.g., electroretinography, ERG).

The leading causes of irreversible blindness in the world are at present photoreceptor degenerative diseases in their many forms (inherited, acquired or induced) and glaucoma. Most clinically identifiable diseases cause blindness through neuronal degeneration of photoreceptors and/or retinal pigment epithelial cells or retinal ganglion cells (RGCs) in the case of retinal degenerative diseases affecting the outer or inner retina, respectively. These diseases are, in many cases, heterogeneous and multifactorial, which complicates the identification of effective treatment, currently non-existent, and therefore represent a major burden on the health system, due to the increase in life expectancy, and also on the economy, as they often affect working-age adults. In addition, it is now widely recognized that photoreceptor degenerations cause, over time, retinal disorganization and complete retinal remodeling, culminating in the degeneration and death of RGCs, the afferent neurons of the retina, which further complicates the success of many of the therapies proposed for these diseases. In addition to retinal neuronal death, it is worth noting the role of retinal glia in the course of these diseases and, in particular, in retinal remodeling and glial seal formation.

This Special Issue aims to study retinal degenerative diseases to shed light on the events that take place in the retina during the course of these diseases, such as neuronal degeneration, glial activation, etc., as well as their possible present and future treatments.

Dr. Diego García-Ayuso
Dr. Johnny Di Pierdomenico
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

  • retina
  • photoreceptor degenerative diseases
  • inherited retinal degenerations
  • glaucoma
  • retinal pigment epithelial cells
  • retinal ganglion cells (RGCs)
  • neuronal degeneration
  • glial activation

Published Papers (2 papers)

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Research

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Article
A Distinct Microglial Cell Population Expressing Both CD86 and CD206 Constitutes a Dominant Type and Executes Phagocytosis in Two Mouse Models of Retinal Degeneration
Int. J. Mol. Sci. 2023, 24(18), 14236; https://doi.org/10.3390/ijms241814236 - 18 Sep 2023
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Abstract
Microglial cells are the key regulators of inflammation during retinal degeneration (RD) and are conventionally classified as M1 or M2. However, whether the M1/M2 classification exactly reflects the functional classification of microglial cells in the retina remains debatable. We examined the spatiotemporal changes [...] Read more.
Microglial cells are the key regulators of inflammation during retinal degeneration (RD) and are conventionally classified as M1 or M2. However, whether the M1/M2 classification exactly reflects the functional classification of microglial cells in the retina remains debatable. We examined the spatiotemporal changes of microglial cells in the blue-LED and NaIO3-induced RD mice models using M1/M2 markers and functional genes. TUNEL assay was performed to detect photoreceptor cell death, and microglial cells were labeled with anti-IBA1, P2RY12, CD86, and CD206 antibodies. FACS was used to isolate microglial cells with anti-CD206 and CD86 antibodies, and qRT-PCR was performed to evaluate Il-10, Il-6, Trem-2, Apoe, and Lyz2 expression. TUNEL-positive cells were detected in the outer nuclear layer (ONL) from 24 h to 72 h post-RD induction. At 24 h, P2RY12 was decreased and CD86 was increased, and CD86/CD206 double-labeled cells occupied the dominant population at 72 h. And CD86/CD206 double-labeled cells showed a significant increase in Apoe, Trem2, and Lyz2 levels but not in those of Il-6 and Il-10. Our results demonstrate that microglial cells in active RD cannot be classified as M1 or M2, and the majority of microglia express both CD86 and CD206, which are involved in phagocytosis rather than inflammation. Full article
(This article belongs to the Special Issue Retinal Degenerative Diseases 2.0)
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Review

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Review
Twenty Years of Anti-Vascular Endothelial Growth Factor Therapeutics in Neovascular Age-Related Macular Degeneration Treatment
Int. J. Mol. Sci. 2023, 24(16), 13004; https://doi.org/10.3390/ijms241613004 - 21 Aug 2023
Cited by 1 | Viewed by 7667
Abstract
Neovascular age-related macular degeneration (nAMD) is the primary disastrous retinal disease that leads to blindness in the elderly population. In the early 2000s, nAMD resulted in irreversible vision loss and blindness with no available treatment options. However, there have been breakthrough advances in [...] Read more.
Neovascular age-related macular degeneration (nAMD) is the primary disastrous retinal disease that leads to blindness in the elderly population. In the early 2000s, nAMD resulted in irreversible vision loss and blindness with no available treatment options. However, there have been breakthrough advances in the drug development of anti-angiogenic biological agents over the last two decades. The primary target molecule for treating nAMD is the vascular endothelial growth factor (VEGF), and there are currently several anti-VEGF drugs such as bevacizumab, ranibizumab, and aflibercept, which have made nAMD more manageable than before, thus preventing vision loss. Nevertheless, it should be noted that these anti-VEGF drugs for nAMD treatment are not effective in more than half of the patients, and even those who initially gain visual improvements lose their vision over time, along with potential deterioration in the geography of atrophy. As a result, there have been continuous endeavors to improve anti-VEGF agents through better efficacy, fewer doses, expanded intervals, and additional targets. This review describes past and current anti-VEGF therapeutics used to treat nAMD and outlines future directions to improve the effectiveness and safety of anti-VEGF agents. Full article
(This article belongs to the Special Issue Retinal Degenerative Diseases 2.0)
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