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Advanced Research in Retina: 3rd Edition
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Advanced Research in Retina: 3rd 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: 30 September 2025 | Viewed by 1975

Special Issue Editors

Dr. Juan J. Salazar

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Guest Editor
Instituto de Investigaciones Oftalmológicas Ramón Castroviejo, Departamento Oftalmología y ORL, Universidad Complutense de Madrid, Madrid, Spain
Interests: retina ganglion cell; intraocular pressure; nerve fibers; retinal; optical coherence tomography; trabeculectomy; glaucoma; anterior eye chamber; ophthalmology
Special Issues, Collections and Topics in MDPI journals
Dr. José A. Fernández-Albarral

E-Mail Website
Guest Editor
Instituto de Investigaciones Oftalmológicas Ramón Castroviejo, Universidad Complutense de Madrid, 28040 Madrid, Spain
Interests: neurophysioly; central nervous system; neuronal and glial cells; neuroinflammation; therapeutical approaches
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The retina is one of the main structures of the eye and is fundamental in the process of seeing. It is also part of the central nervous system (CNS), as it is an extension of the brain.

As a fundamental structure in the visual process, the retina is involved in several pathologies that affect vision and cause blindness, including age-related macular degeneration, diabetic retinopathy, and glaucoma, among others. Therefore, advances in research regarding the pathogenic mechanisms of these diseases and their treatments could represent a major advancement in the control of these retinal pathologies.

As part of the central nervous system, the retina can undergo pathological changes related to neurodegenerative processes such as Alzheimer's disease (AD), Parkinson's disease (PD), and amyotrophic lateral sclerosis (ALS), among others. Thanks to its accessibility and the development of non-invasive imaging techniques, the retina is now considered a biomarker for studying these neurodegenerative pathologies. Therefore, the study of the involvement of the retina in neurodegenerative pathologies, as well as the monitoring of their progression and possible treatments, could represent important advances in the future diagnosis and therapy of these neurodegenerative pathologies.

This Special Issue aims to provide a research platform for the collection of recent original and review articles that address the pathogenic mechanisms of diverse retinal pathologies, innovative diagnostic techniques, and the development of new therapeutic strategies. It will also include articles that investigate retinal alterations in neurodegenerative diseases (AD, PD, ALS, among others), the development of new diagnostic techniques using the retina, and the monitoring of new treatments through the retina.

Dr. Juan J. Salazar
Dr. José A. Fernández-Albarral
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

  • glaucoma
  • age-related macular degeneration
  • diabetic retinopathy
  • neurodegenerative diseases
  • diagnostic techniques
  • therapeutic strategies

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Related Special Issues

Published Papers (3 papers)

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18 pages, 3115 KiB  
Article
Introducing a Porcine Inflammatory Ex Vivo Retina Model for Diabetic Retinopathy
by Agnes Mühle, Sven Schnichels and José Hurst
Int. J. Mol. Sci. 2025, 26(8), 3919; https://doi.org/10.3390/ijms26083919 - 21 Apr 2025
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Abstract
This study aimed to develop an ex vivo retinal model to examine inflammatory processes in diabetic retinopathy (DR) without animal testing. Porcine eyes were collected from a local abattoir, dissected, and cultivated for four days in five experimental groups: control group (Co), 25 [...] Read more.
This study aimed to develop an ex vivo retinal model to examine inflammatory processes in diabetic retinopathy (DR) without animal testing. Porcine eyes were collected from a local abattoir, dissected, and cultivated for four days in five experimental groups: control group (Co), 25 mM and 50 mM mannitol groups (Man25, Man50) as osmotic controls, and 25 mM and 50 mM glucose groups (Glc25, Glc50) as diabetic groups. A TUNEL assay was used to determine relative cell death. Immunofluorescence and quantitative real-time polymerase chain reaction (qRT-PCR) were performed to detect inflammatory markers. An increase in the cell death rate in Man50 (30%), Glc25 (36%) and Glc50 (37%) compared to Co (12%) (p < 0.01, p < 0.001, p < 0.001, respectively) and between Glc25 and Man25 (21%) (p < 0.01) was found. Immunofluorescence staining and qRT-PCR analysis revealed a TNF-α increase in Glc25 compared to Man25 and Co. iNOS was increased in Glc25 vs. Man25 but not in Co vs. Glc25. iNOS gene expression was upregulated with Glc25 treatment compared to Co and Man25 groups. Expression levels of IL-6 and CD31 were significantly higher in Glc25 than in Co and Man25. Glucose treatment increased cell death and inflammation, prompting us to present a DR model for better understanding DR and testing new therapies. Full article
(This article belongs to the Special Issue Advanced Research in Retina: 3rd Edition)
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20 pages, 5919 KiB  
Article
Sustained Experimental Myopia Exacerbates the Effect of Eye Growth on Retinal Ganglion Cell Density and Function
by Carol Ren Lin, Reynolds Kwame Ablordeppey and Alexandra Benavente-Perez
Int. J. Mol. Sci. 2025, 26(6), 2824; https://doi.org/10.3390/ijms26062824 - 20 Mar 2025
Viewed by 520
Abstract
The aim of this study is to describe the effect that sustained myopic eye growth has on the cellular distribution and function of retinal ganglion cells as myopia progresses over time. Ganglion cell density and the photopic negative response (PhNR) were assessed using [...] Read more.
The aim of this study is to describe the effect that sustained myopic eye growth has on the cellular distribution and function of retinal ganglion cells as myopia progresses over time. Ganglion cell density and the photopic negative response (PhNR) were assessed using immunochemistry and electroretinography (ERG), respectively, on twelve common marmoset eyes (Callithrix jacchus). Myopia was induced in six eyes using negative defocus (three eyes from 2 to 6 months of age, 6-month-old myopes; three eyes from 2 to 12 months of age, 12-month-old myopes). These six treated eyes were compared to six age-matched control eyes. Marmosets induced with myopia for four months showed a reduced pan-retinal ganglion cell density, which continued to decrease in the peripapillary area of marmosets induced with sustained myopia for ten months. Ganglion cell density decreased as a function of axial length. Full-field ERGs revealed a dampening of the PhNR in the 12-month-old, but not 6-month-old myopes. The myopic changes observed in ganglion cell density and retinal function suggest a reorganization of the ganglion cell template during myopia development and progression that increases over time with sustained myopic eye growth and translates into functional alterations at later stages of myopia development in the absence of degenerative changes. It remains unknown whether these changes positively or negatively impact retinal function and health. Full article
(This article belongs to the Special Issue Advanced Research in Retina: 3rd Edition)
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21 pages, 7648 KiB  
Article
CX3CR1–Fractalkine Dysregulation Affects Retinal GFAP Expression, Inflammatory Gene Induction, and LPS Response in a Mouse Model of Hypoxic Retinopathy
by Colin Rorex, Sandra M. Cardona, Kaira A. Church, Derek Rodriguez, Difernando Vanegas, Reina A. Saldivar, Amira El-Sheikh, Yufeng Wang, Stefka Gyoneva, Anne C. Cotleur and Astrid E. Cardona
Int. J. Mol. Sci. 2025, 26(3), 1131; https://doi.org/10.3390/ijms26031131 - 28 Jan 2025
Viewed by 1022
Abstract
Diabetic retinopathy (DR) causes vision loss due to sustained inflammation and vascular damage. The vascular damage is evident by fibrinogen leakage, angiogenesis, and hypoxia. Neuronal regulation of microglia via the CX3CL1 (Fractalkine or FKN)-CX3CR1 pathway plays a significant role in retinal pathology. Defects [...] Read more.
Diabetic retinopathy (DR) causes vision loss due to sustained inflammation and vascular damage. The vascular damage is evident by fibrinogen leakage, angiogenesis, and hypoxia. Neuronal regulation of microglia via the CX3CL1 (Fractalkine or FKN)-CX3CR1 pathway plays a significant role in retinal pathology. Defects in FKN or CX3CR1 exacerbate inflammation, vascular damage, and vision impairment. However, the contribution of hypoxic astrocytes to the pathological process of DR is unclear. A hypoxic model (7 days of systemic 7.5% O2) was utilized to induce retinal damage in adult mice in the absence of systemic inflammatory signals. This model induced vascular and microglial responses similar to 10 weeks of STZ-induced hyperglycemia. The goal of this study is to characterize retinal damage in WT and mice with defects in the FKN-CX3CR1 signaling axis and hence assess the impact of the microglial inflammatory responses to hypoxic retinopathy. Tissues were analyzed by immunostaining, RNA sequencing, and cytokine quantification. We found that CX3CR1 deficiency in hypoxic animals induced reactive astrogliosis and that Müller glial responses to hypoxia and systemic inflammation were dependent on FKN signaling. Exacerbated microglial reactivity to hypoxic conditions significantly altered the expression of HIF transcripts. Microglial dysregulation was found to reduce the anti-inflammatory response to hypoxic conditions, downregulate hypoxia-responsive gene expression, and restrained LPS-induced inflammatory responses. We found that microglia dysregulation alters the hypoxic response by inhibiting the upregulation of HIF2α/3α, increasing CD31 immunoreactivity, and altering the expression of ECM-associated transcripts such as type I, III, and XVIII collagens to hypoxic conditions. Full article
(This article belongs to the Special Issue Advanced Research in Retina: 3rd Edition)
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