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Cells
Special Issues
Advances in the Discovery of Retinal Degeneration
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Advances in the Discovery of Retinal Degeneration

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: 20 September 2025 | Viewed by 1573

Special Issue Editors

Dr. Ram Prasad

E-Mail
Guest Editor
Department of Ophthalmology and Visual Sciences, University of Alabama at Birmingham, Birmingham, AL, USA
Interests: retinal cell biology; diabetic retinopathy; photoreceptors; oxidative stress; inflammation; blood–retinal barriers
Special Issues, Collections and Topics in MDPI journals
Dr. Yvonne Adu-Rutledge

E-Mail Website
Guest Editor
Massachusetts Eye and Ear, Harvard Medical School, Boston, MA, USA
Interests: diabetic retinopathy; clinical eye research; inherited retinal diseases inflammation; ocular immunology; blood–retinal barrier changes

Special Issue Information

Dear Colleagues,

Recent years have seen significant advancements in the understanding and treatment of retinal degeneration, a group of conditions leading to progressive vision loss and blindness. The field has evolved rapidly, driven by groundbreaking discoveries in genetic research, novel imaging techniques and innovative therapeutic approaches.

High-throughput sequencing technologies and genome-wide association studies have enabled researchers to pinpoint the specific genes and pathways involved in these disorders, offering new targets for therapeutic intervention. Pharmacological approaches targeting the molecular pathways implicated in retinal degeneration have also made strides. Drugs designed to modulate oxidative stress, inflammation and apoptosis are currently being explored, with some showing promising results in preclinical and early clinical studies.

Given these significant advances, the field of retinal degeneration is ripe for further research and discovery. We invite scientists to contribute their cutting-edge research to our journal's Special Issue, providing a platform to share their findings and drive the next wave of innovation in understanding and treating retinal degeneration. Your contributions will not only enrich the scientific community, but also pave the way for improved therapeutic options for patients suffering from these debilitating conditions.

Dr. Ram Prasad
Dr. Yvonne Adu-Rutledge
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. Cells is an international peer-reviewed open access semimonthly 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 2700 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 cell biology
  • photoreceptors
  • oxidative stress
  • inflammation
  • blood–retinal barriers
  • diabetic retinopathy
  • clinical eye research
  • inherited retinal diseases
  • ocular immunology

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (2 papers)

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16 pages, 5043 KiB  
Article
Adaptive Optics-Transscleral Flood Illumination Imaging of Retinal Pigment Epithelium in Dry Age-Related Macular Degeneration
by Laura Kowalczuk, Rémy Dornier, Aurélie Navarro, Fanny Jeunet, Christophe Moser, Francine Behar-Cohen and Irmela Mantel
Cells 2025, 14(9), 633; https://doi.org/10.3390/cells14090633 - 24 Apr 2025
Viewed by 205
Abstract
Adaptive optics-transscleral flood illumination (AO-TFI) is a novel imaging technique with potential for detecting retinal pigment epithelium (RPE) changes in dry age-related macular degeneration (AMD). This single-center prospective study evaluated its ability to visualize pathological features in AMD. AO-TFI images were acquired using [...] Read more.
Adaptive optics-transscleral flood illumination (AO-TFI) is a novel imaging technique with potential for detecting retinal pigment epithelium (RPE) changes in dry age-related macular degeneration (AMD). This single-center prospective study evaluated its ability to visualize pathological features in AMD. AO-TFI images were acquired using the prototype Cellularis® camera over six 5 × 5° macular zones in patients with good fixation and no exudative changes. Conventional imaging modalities, including spectral-domain optical coherence tomography (OCT), color fundus photography and fundus autofluorescence, were used for comparison. AO-TFI images were correlated with OCT using a custom method (Fiji software, v. 2.9). Eleven eyes of nine patients (70 ± 8.3 years) with early (n = 5), intermediate (n = 1) and atrophic (n = 5) AMD were analyzed. AO-TFI identified relevant patterns in dry AMD. RPE cell visibility was impaired in affected eyes, but AO-TFI distinguished cuticular drusen with hyporeflective centers and bright edges, large ill-defined drusen and stage 3 subretinal drusenoid deposits as prominent hyperreflective spots. It provided superior resolution for small drusen compared to OCT and revealed crystalline structures and hyporeflective dots in atrophic regions. Atrophic borders remained isoreflective unless RPE displacement was absent, allowing precise delineation. These findings highlight AO-TFI’s potential as a sensitive imaging tool for characterizing early AMD and clinical research. Full article
(This article belongs to the Special Issue Advances in the Discovery of Retinal Degeneration)
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18 pages, 5278 KiB  
Article
Novel mTORC2/HSPB4 Interaction: Role and Regulation of HSPB4 T148 Phosphorylation
by Zachary B. Sluzala, Yang Shan, Lynda Elghazi, Emilio L. Cárdenas, Angelina Hamati, Amanda L. Garner and Patrice E. Fort
Cells 2024, 13(23), 2000; https://doi.org/10.3390/cells13232000 - 4 Dec 2024
Cited by 1 | Viewed by 966
Abstract
HSPB4 and HSPB5 (α-crystallins) have shown increasing promise as neuroprotective agents, demonstrating several anti-apoptotic and protective roles in disorders such as multiple sclerosis and diabetic retinopathy. HSPs are highly regulated by post-translational modification, including deamidation, glycosylation, and phosphorylation. Among them, T148 phosphorylation has [...] Read more.
HSPB4 and HSPB5 (α-crystallins) have shown increasing promise as neuroprotective agents, demonstrating several anti-apoptotic and protective roles in disorders such as multiple sclerosis and diabetic retinopathy. HSPs are highly regulated by post-translational modification, including deamidation, glycosylation, and phosphorylation. Among them, T148 phosphorylation has been shown to regulate the structural and functional characteristics of HSPB4 and underlie, in part, its neuroprotective capacity. We recently demonstrated that this phosphorylation is reduced in retinal tissues from patients with diabetic retinopathy, raising the question of its regulation during diseases. The kinase(s) responsible for regulating this phosphorylation, however, have yet to be identified. To this end, we employed a multi-tier strategy utilizing in vitro kinome profiling, bioinformatics, and chemoproteomics to predict and discover the kinases capable of phosphorylating T148. Several kinases were identified as being capable of specifically phosphorylating T148 in vitro, and further analysis highlighted mTORC2 as a particularly strong candidate. Altogether, our data demonstrate that the HSPB4-mTORC2 interaction is multi-faceted. Our data support the role of mTORC2 as a specific kinase phosphorylating HSPB4 at T148, but also provide evidence that the HSPB4 chaperone function further strengthens the interaction. This study addresses a critical gap in our understanding of the regulatory underpinnings of T148 phosphorylation-mediated neuroprotection. Full article
(This article belongs to the Special Issue Advances in the Discovery of Retinal Degeneration)
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