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Advanced Research in Retina: 3rd Edition

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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

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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

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Keywords

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

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Published Papers (1 paper)

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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 385
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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