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Medicina
Special Issues
Retinal Diseases: Clinical Presentation and Novel Treatments
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Retinal Diseases: Clinical Presentation and Novel Treatments

A special issue of Medicina (ISSN 1648-9144). This special issue belongs to the section "Ophthalmology".

Deadline for manuscript submissions: 31 August 2024 | Viewed by 3571

Special Issue Editors

Dr. Joshua Ong

E-Mail Website
Guest Editor
Department of Ophthalmology and Visual Sciences, University of Michigan Kellogg Eye Center, Ann Arbor, MI 48105, USA
Interests: ophthalmology; artificial intelligence; space medicine; optical coherence tomography; machine learning
Dr. Jay Chhablani

E-Mail Website
Guest Editor
UPMC Eye Center, University of Pittsburgh, Pittsburgh, PA 15213, USA
Interests: retinal imaging; central serous chorioretinopathy; optic disc pit
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The retina plays a critical role in vision and quality of life. Preserving the retina in aging and disease is of the utmost importance. Within the past decade, therapies and imaging techniques for retinal diseases have emerged. Advances in imaging, including various optical coherence tomography (OCT) techniques, OCT angiography, multi confocal scanning laser ophthalmoscopy (MCSLO), and adaptive optics, have revolutionized how we can detect and understand retinal disease presentation. Various therapies that have revolutionized retinal disease management have also been introduced, such as multiple anti-VEGF intravitreal injection therapies for neovascular age-related macular degeneration. Research has also focused on various treatments, including gene therapy, complement component targeting, episcleral brachytherapy, subthreshold micropulse laser, and port delivery systems.

We are pleased to invite you to submit your work for a new Special Issue entitled “Retinal Diseases: Clinical Presentation and Novel Treatments”. We welcome the submission of original research articles or reviews that discuss the recent advances in understanding the clinical presentation of retinal disease and/or the novel treatments that have emerged for these diseases.

Dr. Joshua Ong
Dr. Jay Chhablani
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. Medicina 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 2200 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

  • retina
  • clinical presentation
  • age-related macular degeneration
  • choroid
  • chorioretinal disease
  • optical coherence tomography
  • novel therapies

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

Published Papers (3 papers)

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Research

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11 pages, 579 KiB  
Article
Deep Learning in Neovascular Age-Related Macular Degeneration
by Enrico Borrelli, Sonia Serafino, Federico Ricardi, Andrea Coletto, Giovanni Neri, Chiara Olivieri, Lorena Ulla, Claudio Foti, Paola Marolo, Mario Damiano Toro, Francesco Bandello and Michele Reibaldi
Medicina 2024, 60(6), 990; https://doi.org/10.3390/medicina60060990 - 17 Jun 2024
Viewed by 819
Abstract
Background and objectives: Age-related macular degeneration (AMD) is a complex and multifactorial condition that can lead to permanent vision loss once it progresses to the neovascular exudative stage. This review aims to summarize the use of deep learning in neovascular AMD. Materials [...] Read more.
Background and objectives: Age-related macular degeneration (AMD) is a complex and multifactorial condition that can lead to permanent vision loss once it progresses to the neovascular exudative stage. This review aims to summarize the use of deep learning in neovascular AMD. Materials and Methods: Pubmed search. Results: Deep learning has demonstrated effectiveness in analyzing structural OCT images in patients with neovascular AMD. This review outlines the role of deep learning in identifying and measuring biomarkers linked to an elevated risk of transitioning to the neovascular form of AMD. Additionally, deep learning techniques can quantify critical OCT features associated with neovascular AMD, which have prognostic implications for these patients. Incorporating deep learning into the assessment of neovascular AMD eyes holds promise for enhancing clinical management strategies for affected individuals. Conclusion: Several studies have demonstrated effectiveness of deep learning in assessing neovascular AMD patients and this has a promising role in the assessment of these patients. Full article
(This article belongs to the Special Issue Retinal Diseases: Clinical Presentation and Novel Treatments)
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<p>Article review and selection process.</p> Full article ">

Review

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30 pages, 4181 KiB  
Review
The Complement System as a Therapeutic Target in Retinal Disease
by Joshua Ong, Arman Zarnegar, Amrish Selvam, Matthew Driban and Jay Chhablani
Medicina 2024, 60(6), 945; https://doi.org/10.3390/medicina60060945 - 5 Jun 2024
Viewed by 1120
Abstract
The complement cascade is a vital system in the human body’s defense against pathogens. During the natural aging process, it has been observed that this system is imperative for ensuring the integrity and homeostasis of the retina. While this system is critical for [...] Read more.
The complement cascade is a vital system in the human body’s defense against pathogens. During the natural aging process, it has been observed that this system is imperative for ensuring the integrity and homeostasis of the retina. While this system is critical for proper host defense and retinal integrity, it has also been found that dysregulation of this system may lead to certain retinal pathologies, including geographic atrophy and diabetic retinopathy. Targeting components of the complement system for retinal diseases has been an area of interest, and in vivo, ex vivo, and clinical trials have been conducted in this area. Following clinical trials, medications targeting the complement system for retinal disease have also become available. In this manuscript, we discuss the pathophysiology of complement dysfunction in the retina and specific pathologies. We then describe the results of cellular, animal, and clinical studies targeting the complement system for retinal diseases. We then provide an overview of complement inhibitors that have been approved by the Food and Drug Administration (FDA) for geographic atrophy. The complement system in retinal diseases continues to serve as an emerging therapeutic target, and further research in this field will provide additional insights into the mechanisms and considerations for treatment of retinal pathologies. Full article
(This article belongs to the Special Issue Retinal Diseases: Clinical Presentation and Novel Treatments)
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<p>Overview of the complement cascade involving the classical, lectin, and alternative pathways to construct the membrane attack complex. Anaphylatoxins (C3a, C4a, and C5a) may trigger inflammatory responses, while regulatory proteins CFH and C59 may modulate the activity of the complement system.</p> Full article ">Figure 2
<p>Complement activation in geographic atrophy. The deterioration of retinal pigment epithelium (RPE) in geographic atrophy (GA) allows for additional complement to access the retina. Complement activation leads to the formation of the membrane attack complex, thus leading to destruction and cell death of photoreceptors and RPE in GA. Figure reprinted with permission from Campagne et al. [<a href="#B41-medicina-60-00945" class="html-bibr">41</a>] under Creative Commons Attribution 4.0 International License (<a href="https://creativecommons.org/licenses/by/4.0/legalcode.en" target="_blank">https://creativecommons.org/licenses/by/4.0/legalcode.en</a>, accessed on 1 March 2024).</p> Full article ">Figure 3
<p>Pathologic changes that precede age-related macular degeneration (AMD). The green section indicates that healthy eyes without CFH Y402H mutations can freely regulate transport of oxygen and other nutrients from the choroidal circulation (circulation) through the blood-retinal barrier and to the RPE and photoreceptors. In eyes with this CFH Y402H mutation, there is a predisposition for AMD (yellow section). The RPE cells exhibit decreased oxidative phosphorylation (ox phos) capacity. In conjunction with natural aging, there is a disruption in transport through the Bruch membrane. Unchecked complement activation occurs depending on the severity of the mutations and the degree of extracellular matrix (ECM) disruption. Oxidative stress induces RPE cell damage, further promoting a pro-inflammatory state by causing cytokine release (IL-6, IL-8). In early stage AMD (red), there is an accumulation of oxidized lipoproteins (drusen) that form in the Bruch membrane. There are degenerative changes in macular RPE cells and photoreceptors. Figure reprinted with permission from Armento et al. [<a href="#B48-medicina-60-00945" class="html-bibr">48</a>] under Creative Commons Attribution 4.0 International License (<a href="https://creativecommons.org/licenses/by/4.0/legalcode.en" target="_blank">https://creativecommons.org/licenses/by/4.0/legalcode.en</a>, accessed on 1 March 2024).</p> Full article ">Figure 4
<p>Natural aging and the progression to late-stage AMD. This figure demonstrates the key stages of AMD progression, beginning with an overview of ocular anatomy (<b>A</b>,<b>B</b>), natural aging processes (<b>C</b>), early/intermediate AMD (<b>D</b>), late-stage non-exudative (dry) AMD (<b>E</b>), and finally late-stage exudative (wet) AMD (<b>F</b>). In natural aging, changes in the Bruch membrane (<b>C</b>) impair the exchange of nutrients for waste, damaging local structures such as the RPE. Inflammatory processes take hold, and the complement system is activated (<b>D</b>). In late-stage disease, there is either widespread RPE atrophy (geographic atrophy) (<b>E</b>) or else CNV network formation (<b>F</b>). Figure reprinted with permission from Armento et al. [<a href="#B48-medicina-60-00945" class="html-bibr">48</a>] under Creative Commons Attribution 4.0 International License (<a href="https://creativecommons.org/licenses/by/4.0/legalcode.en" target="_blank">https://creativecommons.org/licenses/by/4.0/legalcode.en</a>, accessed on 1 March 2024).</p> Full article ">Figure 5
<p>Geographic atrophy visualized using different imaging modalities. Box (<b>A</b>) demonstrates multicolor imaging showing reflectance in different wavelengths in geographic atrophy. Box (<b>B</b>) demonstrates fundus autofluorescence, showing geographic atrophy as sharply demarcated dark regions. Box (<b>C</b>) shows infrared reflectance with an adjacent optical coherence tomography (OCT) B-scan of the central fovea, showing the loss of outer retinal layers and retinal pigment epithelium. Box (<b>D</b>) demonstrates en face OCT angiography, showing loss of flow at the choriocapillaris within the lesion. Box (<b>E</b>) demonstrates en face OCT, showing hyper-reflectance at the choriocapillaris layer due to backscattering. Box (<b>F</b>) demonstrates an OCT angiography B-scan of the central fovea showing loss of flow in the choriocapillaris. Reprinted with permission from Sacconi et al. [<a href="#B163-medicina-60-00945" class="html-bibr">163</a>] under Creative Commons Attribution-NonCommercial 4.0 International License (<a href="https://creativecommons.org/licenses/by-nc/4.0/legalcode.en" target="_blank">https://creativecommons.org/licenses/by-nc/4.0/legalcode.en</a>, accessed on 1 March 2024).</p> Full article ">
15 pages, 1105 KiB  
Review
Microbial Dynamics in Ophthalmic Health: Exploring the Interplay between Human Microbiota and Glaucoma Pathogenesis
by Joicye Hernández-Zulueta, Andres J. Bolaños-Chang, Francisco J. Santa Cruz-Pavlovich, América D. Valero Rodríguez, Alejandro Lizárraga Madrigal, Ximena I. Del Rio-Murillo, José Navarro-Partida and Alejandro Gonzalez-De la Rosa
Medicina 2024, 60(4), 592; https://doi.org/10.3390/medicina60040592 - 3 Apr 2024
Viewed by 1215
Abstract
The human microbiome has a crucial role in the homeostasis and health of the host. These microorganisms along with their genes are involved in various processes, among these are neurological signaling, the maturation of the immune system, and the inhibition of opportunistic pathogens. [...] Read more.
The human microbiome has a crucial role in the homeostasis and health of the host. These microorganisms along with their genes are involved in various processes, among these are neurological signaling, the maturation of the immune system, and the inhibition of opportunistic pathogens. In this sense, it has been shown that a healthy ocular microbiota acts as a barrier against the entry of pathogens, contributing to the prevention of infections. In recent years, a relationship has been suggested between microbiota dysbiosis and the development of neurodegenerative diseases. In patients with glaucoma, it has been observed that the microbiota of the ocular surface, intraocular cavity, oral cavity, stomach, and gut differ from those observed in healthy patients, which may suggest a role in pathology development, although the evidence remains limited. The mechanisms involved in the relationship of the human microbiome and this neurodegenerative disease remain largely unknown. For this reason, the present review aims to show a broad overview of the influence of the structure and composition of the human oral and gut microbiota and relate its dysbiosis to neurodegenerative diseases, especially glaucoma. Full article
(This article belongs to the Special Issue Retinal Diseases: Clinical Presentation and Novel Treatments)
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<p>Overview of the relationship between microbiome alterations and glaucoma development. In individuals diagnosed with glaucoma, there is a noticeable shift in the relative abundance of various microorganisms within specific sites, including the ocular, oral, and gut microenvironments. The influence of any single bacterium is overshadowed by the overall collective presence of the microbial population. Localized inflammation triggered by this bacterial presence, alongside additional factors such as adipose tissue levels, dietary habits, and age, contributes to the disruption of cellular barriers and tight junctions. Consequently, bacteria breach these constraints, prompting the activation of the immune system. This immune response involves the mobilization of immune cells and the complement system in reaction to bacterial components such as lipopolysaccharides, culminating in systemic inflammation. This inflammatory process is known to compromise the integrity of the blood–retinal and blood–aqueous barriers, allowing the invasion of both bacteria and immunological constituents, including T-cells previously sensitized to bacterial elements such as heat shock proteins, which exhibit molecular mimicry with host antigens. Subsequent immunological activation within the ocular environment exceeds its innate regulatory capacity, fostering various pathological alterations that ultimately lead to the degeneration of retinal ganglion cells and loss of axons. BDNF, brain-derived neurotrophic factor; bFGF; basic fibroblast growth factor; CNTF, ciliary neurotrophic factor; GDNF, glial cell line-derived neurotrophic factor; HSP, heat shock proteins; IFN-a, interferon alpha; LPS, lipopolysaccharides; miR, microRNA; NF-κB, nuclear factor kappa-light-chain-enhancer of activated B cells; NGF, nerve growth factor; NT3, neurotrophin-3; RGC, retinal ganglion cell; TLR-4, Toll-like receptor 4; NF-κB.</p> Full article ">
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