Neuroinflammation in Ocular Diseases: Emerging Insights into Mechanisms, Biomarkers, and Therapeutic Targets

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

Deadline for manuscript submissions: 31 May 2025 | Viewed by 1452

Special Issue Editor


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Guest Editor
Clinical and Administrative Pharmacy, University of Georgia, Augusta, GA 30912, USA
Interests: retina; ischemic retinopathy; neurovascular injury; neurodegeneration; oxidative stress; polyamine oxidase
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neuroinflammation is increasingly recognized as a critical component in ocular diseases, including diabetic retinopathy, glaucoma, optic neuritis, and optic neuropathies. These diseases impact millions of individuals globally and present complex and multifaceted pathologies affecting the retina, optic nerve, or both. The precise mechanisms driving neuroinflammation in these conditions are still not fully understood, complicating efforts to develop effective therapies.  This Special Issue is dedicated to advancing our knowledge of the neuroinflammatory processes in ocular diseases. We seek to highlight recent breakthroughs in understanding the mechanisms and efforts to identify novel biomarkers and therapeutic targets. By fostering research in these areas, we aim to contribute to the development of innovative, targeted treatments that could significantly improve outcomes for patients affected by these challenging conditions.

Dr. S. Priya Narayanan
Guest Editor

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Keywords

  • neuroinflammation
  • vision
  • retina
  • optic nerve
  • neurodegeneration
  • inflammation
  • biomarker
  • therapeutic strategies
  • pharmacological treatments

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Published Papers (1 paper)

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Research

24 pages, 9433 KiB  
Article
Targeting SMOX Preserves Optic Nerve Myelin, Axonal Integrity, and Visual Function in Multiple Sclerosis
by Harry O. Henry-Ojo, Fang Liu and S. Priya Narayanan
Biomolecules 2025, 15(2), 158; https://doi.org/10.3390/biom15020158 - 21 Jan 2025
Viewed by 1196
Abstract
Multiple sclerosis (MS) is a highly disabling chronic neurological condition affecting young adults. Inflammation, demyelination, and axonal damage are key pathological features of MS and its animal model, experimental autoimmune encephalomyelitis (EAE). Our previous work demonstrated that inhibiting spermine oxidase (SMOX) with MDL72527, [...] Read more.
Multiple sclerosis (MS) is a highly disabling chronic neurological condition affecting young adults. Inflammation, demyelination, and axonal damage are key pathological features of MS and its animal model, experimental autoimmune encephalomyelitis (EAE). Our previous work demonstrated that inhibiting spermine oxidase (SMOX) with MDL72527, a selective irreversible pharmacological inhibitor, significantly reduced clinical symptoms, retinal ganglion cell (RGC) loss, and optic nerve inflammation in EAE mice. The present study explored the broader therapeutic potential of SMOX inhibition, focusing on myelin preservation, axonal integrity, and visual function in the EAE model. Electron microscopy of optic nerve cross-sections showed significant preservation of myelin thickness and axonal integrity due to SMOX inhibition. The quantitative assessment showed that g-ratio and axon count metrics were significantly improved in MDL72527-treated EAE mice compared to their vehicle-treated counterparts. Immunofluorescence studies confirmed these findings, showing increased preservation of myelin and axonal proteins in MDL72527-treated EAE mice compared to the vehicle-treated group. Functional assessment studies (Electroretinography) demonstrated significant improvement in RGC function and axonal conduction in EAE mice treated with MDL72527. Furthermore, SMOX inhibition downregulated the expression of galectin3 (Gal3), a mediator of neuroinflammation, indicating Gal3’s role in SMOX-mediated neuroprotection. This study provides compelling evidence for the potential of SMOX inhibition as a therapeutic strategy in multiple sclerosis and other demyelinating disorders. Full article
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