From Molecular Mechanisms to Therapies: Advances in Retinal Disease Research

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (31 March 2026) | Viewed by 799

Special Issue Editors

Special Issue Information

Dear Colleagues,

We would like to invite you to contribute to this Special Issue by submitting review articles that provide the most advanced information about the molecular causes of retinal diseases, in addition to the most developed therapeutic approaches for the retinal pathologies.

The retina is a fundamental tissue of the eye that makes it possible to transform the electrochemical stimuli elicited from the light into images through transporting the signal to the visual cortex. During aging, the retina tends to degenerate in a large portion of the population, leading to the onset of different retinal diseases (RDs). These conditions can result in loss of retinal function, which progresses into blindness.

It has been estimated that worldwide, between 7 and 8 million people are blind due to retinal diseases (accounting for overlaps and primary cause classifications). Additionally, over 13 million people suffer from severe vision impairment (MSVI) due to these conditions. The main contributing conditions are diabetic retinopathy, AMD, glaucoma, and retinitis pigmentosa.

In this Special Issue, we would like to highlight the latest knowledge about the molecular (genetic, biochemical and epigenetic) causes leading to these retinal pathologies and the new potential therapeutic approaches.

Dr. Marco Feligioni
Dr. Maccarone Rita
Guest Editors

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Keywords

  • retinal diseases
  • retinal pathologies
  • preclinical studies

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Published Papers (1 paper)

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Research

16 pages, 4837 KB  
Article
Resilience to Diabetic Retinopathy (RDR) Is Associated with a Pre-Retinopathy Transcriptional Program Induced by Diabetes
by Janani Rajasekar, Maria Paula Zappia, Maximilian A. McCann, Maxim V. Frolov and Andrius Kazlauskas
Biomolecules 2026, 16(4), 614; https://doi.org/10.3390/biom16040614 - 21 Apr 2026
Viewed by 474
Abstract
The purpose of this project was to define gene expression changes associated with the acquisition and loss of resilience to diabetic retinopathy (RDR) in individual retinal cell types. A non-immune form of type 1 diabetes mellitus (DM) was induced by injecting male C57Bl6J [...] Read more.
The purpose of this project was to define gene expression changes associated with the acquisition and loss of resilience to diabetic retinopathy (RDR) in individual retinal cell types. A non-immune form of type 1 diabetes mellitus (DM) was induced by injecting male C57Bl6J mice with streptozotocin. Single-cell RNA sequencing was performed on retinas from mice that experienced DM for 5 or 15 days, along with retinas from age-matched, non-DM mice. The resulting data sets were analyzed to identify DM-associated differentially expressed genes and pathway enrichments after each duration of DM. We observed that acquisition of RDR, previously shown to arise after 5 days of DM was linked to altered expression of genes in a subset of retinal cells, mainly Müller cells. Pathway analysis indicated enhancement of numerous modes of protection, including reinforced neurovascular and structural homeostasis through phagocytosis, integrin signaling, and interferon-mediated defense. After 15 days of DM, when we previously showed that RDR is waning this pro-protection surge in gene expression subsided. We conclude that a duration of DM that is too short to cause diabetic retinopathy (DR) nonetheless evoked a profound change in the gene expression profile within a subset of retinal cell types. The nature and timing of this molecular shift indicated that it was not the preamble to DM-related damage that eventually develops. Rather, DM engaged numerous defense programs within Müller cells. The temporal alignment between RDR and activation of Müller cell-based defense provides a molecular foundation for the retina’s transient ability to remain healthy in the face of DM. Full article
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