ArticleJournal of neuroinflammation2025
Targeting glial fibrillary acidic protein in glaucoma: a monoclonal antibody approach to modulate glial reactivity and neuroinflammation for neuroprotection.
Article in Journal of neuroinflammation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- [Progress on prognostic assessment methods for mild cognitive impairment].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2026Review
- Cargo molecules in plasma neural-derived extracellular vesicles reveal pathological signatures of primary open-angle glaucoma.Journal of translational medicine · 2026Article
- Review
- A Freshwater Pearl Mussel Polysaccharide Alleviates Inflammatory Pain by Targeting Peripheral Cytokines and Spinal Astroglial NLRP3/GFAP Responses.Food science & nutrition · 2026Article
- Plasma GFAP and NLRP3 Associate with Cognitive Impairment After Recent Small Subcortical Infarct via Periventricular White Matter Hyperintensity.CNS neuroscience & therapeutics · 2026Article
- In Vivo Functional and Structural Retinal Preservation by Combined Administration of Citicoline and Coenzyme Q10 in a Murine Model of Ocular Hypertension.International journal of molecular sciences · 2026Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGlaucoma is a progressive neurodegenerative disorder that leads to irreversible vision loss, with neuroinflammation recognized as a key factor. Overexpression of glial fibrillary acidic protein (GFAP) is linked to glaucoma pathogenesis and plays a pivotal role in astrocyte-driven neuroinflammation. This study aimed to assess the neuroprotective effects of a monoclonal antibody (mAb) targeting GFAP in glaucoma and to elucidate the underlying mechanisms.
methodsAn ocular hypertension (OHT) glaucoma model was established in female Sprague Dawley rats using episcleral vein occlusion. Three doses of GFAP mAb (2.5, 25, 50 µg) or vehicle were administered via intravitreal injection. Retinal nerve fiber layer (RNFL) thickness and photopic electroretinogram were monitored longitudinally. Retinal ganglion cell (RGC) survival and glial responses were evaluated with immunostaining. Western blot and microarray analyses were performed to investigate molecular and pathway alterations. Additionally, a cobalt chloride (CoCl
resultsOHT resulted in a significant loss of RNFL thickness, PhNR amplitude, and RGC survival, all of which were preserved by GFAP mAb treatment. Retinal astrocyte reactivity was inhibited by GFAPmAb in a dose-dependent manner by suppressing GFAP protein overexpression. Notably, 25 µg GFAP mAb effectively regulated both astrocyte and microglial reactivity, leading to a substantial attenuation of neuroinflammation. Mechanistically, GFAP mAb inhibited the p38 MAPK and NF-κB pathways and the NLRP3/Caspase-1/GSDMD axis. In vitro, GFAP mAb improved R28 cell viability under CoCl
conclusionsThis study demonstrates that GFAP mAb inhibits astrogliosis and glial-glial activation, exerting neuroprotection through the inhibition of inflammation and pyroptosis. The findings suggest that targeting GFAP represents a promising immunotherapeutic strategy for glaucoma treatment.
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