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Molecular Mechanisms of Retinal Diseases: An Update
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Molecular Mechanisms of Retinal Diseases: An Update

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 3263

Special Issue Editor

Dr. Yukihiro Shiga

E-Mail Website
Guest Editor
Department of Neuroscience, University of Montreal Hospital Research Centre (CRCHUM), Montreal, QC H3G 1A4, Canada
Interests: glaucoma; retinal ganglion cells; clinical ophthalmology; eye diseases; retinal imaging; visual neuroscience

Special Issue Information

Dear Colleagues, 

This Special Issue is supervised by Dr. Yukihiro Shiga and assisted by our Topical Advisory Panel Member Francesco Saverio (Ospedale Maggiore, Bologna, Italy).

Homeostatic processes of retinal structure and function are orchestrated by neurons, glial cells, and vasculature; their disruption leads to remodeling and degeneration in the pathophysiology of vision-threatening retinal diseases.

Recent advances in molecular biology have enabled state-of-the-art imaging techniques by using multiphoton microscopy, genome editing by using the CRISPR/Cas9 system, novel disease modeling by using iPS cells, and multi-omics analyses, including single-cell RNA seq.

The above have allowed for the visualization of molecular dynamics in vivo, the establishment of disease-specific genetic modifications as well as models, and an understanding of complex intracellular diversity, resulting in the identification of promising molecules that cause critical pathologies and the determination of therapeutic strategies with which to restore damaged tissues and their functions.

This Special Issue aims to discuss and summarize insights into new molecular mechanisms and potential therapeutics for retinal degenerative diseases, such as age-related macular degeneration, diabetic retinopathy, inherited retinal diseases, glaucoma, myopia, and retinal vascular diseases.

In this Special Issue, we welcome original research or review articles on the pathogenesis of retinal diseases and their therapeutic targets via the use of novel molecular biological approaches.

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

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Keywords

  • in vivo imaging
  • CRISPR/Cas9
  • iPS cells
  • single-cell RNA seq
  • age-related macular degeneration
  • diabetic retinopathy
  • inherited retinal diseases
  • glaucoma
  • myopia
  • retinal vascular diseases

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Published Papers (3 papers)

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Research

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18 pages, 11934 KiB  
Article
Bim Expression Influences Choroidal Endothelial Cell Characteristics and Their Response to Therapeutic Intervention
by Nader Sheibani, Yong-Seok Song, Mitra Farnoodian, Samay Inampudi, Barbara Hanna, Shoujian Wang, Soesiawati R. Darjatmoko and Christine M. Sorenson
Int. J. Mol. Sci. 2024, 25(19), 10254; https://doi.org/10.3390/ijms251910254 - 24 Sep 2024
Viewed by 636
Abstract
In the aging population, choroidal vessels grow through the Bruch’s membrane, resulting in a loss of central vision due to choroidal neovascularization (CNV). During active neovascularization, CNV is associated with inappropriate levels of apoptosis in multiple cell types, including choroidal endothelial cells (ChECs). [...] Read more.
In the aging population, choroidal vessels grow through the Bruch’s membrane, resulting in a loss of central vision due to choroidal neovascularization (CNV). During active neovascularization, CNV is associated with inappropriate levels of apoptosis in multiple cell types, including choroidal endothelial cells (ChECs). Bim is a pro-apoptotic member of the Bcl-2 family. It is essential for cell apoptosis due to exposure to drugs such as dexamethasone or decreased pro-survival factors, including vascular endothelial growth factor (VEGF). To better elucidate the cell autonomous contribution of Bim expression in the integrity and neovascularization of the choroidal vasculature, we isolated ChECs from wild-type and Bim-deficient (Bim−/−) mice. ChECs lacking Bim expression demonstrated increased expression of VEGF, osteopontin, and the inflammatory cytokines Rantes/Ccl5 and IL6. Bim−/− ChECs were more proliferative and demonstrated an increased capacity to undergo capillary morphogenesis. Anti-VEGF had a diminished capacity to disrupt capillary morphogenesis in Bim−/− ChECs. In vivo, utilizing the mouse laser photocoagulation model, anti-VEGF treatment mitigated CNV in wild-type but not Bim−/− mice. We also tested other modalities that are thought to not require the intrinsic death pathway for their function and showed that propranolol, anti-CTGF, and the TSP1-mimetic peptide ABT898 mitigated CNV in mice lacking Bim expression to varying degrees. Thus, in ChECs, Bim expression could impact the effectiveness of treatment modalities that require the intrinsic death pathway to mitigate CNV. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Retinal Diseases: An Update)
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13 pages, 3579 KiB  
Article
JP4-039, a Mitochondria-Targeted Nitroxide, Mitigates the Effect of Apoptosis and Inflammatory Cell Migration in the Irradiated Mouse Retina
by Jennifer O. Adeghate, Michael W. Epperly, Katherine Anne Davoli, Kira L. Lathrop, Peter Wipf, Wen Hou, Renee Fisher, Stephanie Thermozier, M. Saiful Huq, Jose-Alain Sahel, Joel S. Greenberger and Andrew W. Eller
Int. J. Mol. Sci. 2024, 25(12), 6515; https://doi.org/10.3390/ijms25126515 - 13 Jun 2024
Viewed by 1400
Abstract
We hypothesize that the injection of JP4-039, a mitochondria-targeted nitroxide, prior to irradiation of the mouse retina may decrease apoptosis and reduce neutrophil and macrophage migration into the retina. In our study, we aimed to examine the effects of JP4-039 in the mouse [...] Read more.
We hypothesize that the injection of JP4-039, a mitochondria-targeted nitroxide, prior to irradiation of the mouse retina may decrease apoptosis and reduce neutrophil and macrophage migration into the retina. In our study, we aimed to examine the effects of JP4-039 in the mouse retina using fluorescent microscopy, a terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay, and flow cytometry. Forty-five mice and one eye per mouse were used. In Group 1, fluorescent microscopy was used to determine retinal uptake of 10 µL (0.004 mg/µL) of intravitreally injected BODIPY-labeled JP4-039 at 0, 15, and 60 min after injection. In Group 2, the TUNEL assay was performed to investigate the rate of apoptosis after irradiation in addition to JP4-039 injection, compared to controls. In Group 3, flow cytometry was used to determine the extent of inflammatory cell migration into the retina after irradiation in addition to JP4-039 injection, compared to controls. Maximal retinal uptake of JP4-039 was 15 min after intravitreal injection (p < 0.0001). JP4-039-treated eyes had lower levels of retinal apoptosis (35.8 ± 2.5%) than irradiated controls (49.0 ± 2.7%; p = 0.0066) and demonstrated reduced migration of N1 cells (30.7 ± 11.7% vs. 77.7 ± 5.3% controls; p = 0.004) and M1 cells (76.6 ± 4.2 vs. 88.1 ± 3.7% controls, p = 0.04). Pretreatment with intravitreally injected JP4-039 reduced apoptosis and inflammatory cell migration in the irradiated mouse retina, marking the first confirmed effect of this molecule in retinal tissue. Further studies may allow for safety profiling and potential use for patients with radiation retinopathy. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Retinal Diseases: An Update)
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Review

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14 pages, 1961 KiB  
Review
Proliferative Vitreoretinopathy in Retinal Detachment: Perspectives on Building a Digital Twin Model Using Nintedanib
by Giacomo Visioli, Annalisa Romaniello, Leonardo Spinoglio, Giuseppe Maria Albanese, Ludovico Iannetti, Oscar Matteo Gagliardi, Alessandro Lambiase and Magda Gharbiya
Int. J. Mol. Sci. 2024, 25(20), 11074; https://doi.org/10.3390/ijms252011074 - 15 Oct 2024
Viewed by 709
Abstract
Proliferative vitreoretinopathy (PVR) is a pathological process characterized by the formation of fibrotic membranes that contract and lead to recurrent retinal detachment. Pars plana vitrectomy (PPV) is the primary treatment, but recurrence rates remain high, as surgery does not address the underlying molecular [...] Read more.
Proliferative vitreoretinopathy (PVR) is a pathological process characterized by the formation of fibrotic membranes that contract and lead to recurrent retinal detachment. Pars plana vitrectomy (PPV) is the primary treatment, but recurrence rates remain high, as surgery does not address the underlying molecular mechanisms driving fibrosis. Despite several proposed pharmacological interventions, no approved therapies exist, partly due to challenges in conducting preclinical and in vivo studies for ethical and safety reasons. This review explores the potential of computational models and Digital Twins, which are increasingly gaining attention in medicine. These tools could enable the development of progressively complex PVR models, from basic simulations to patient-specific Digital Twins. Nintedanib, a tyrosine kinase inhibitor targeting PDGFR, VEGFR, and FGFR, is presented as a prototype for computational models to simulate its effects on fibrotic pathways in virtual patient cohorts. Although still in its early stages, the integration of computational models and Digital Twins offers promising avenues for improving PVR management through more personalized therapeutic strategies. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Retinal Diseases: An Update)
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