ArticleMolecular neurobiology2025
Inhibition of Vascular Endothelial Growth Factor Reduces Photoreceptor Death in Retinal Neovascular Disease via Neurotrophic Modulation in Müller Glia.
Article in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed.
- VEGFR2 deletion increases susceptibility to photoreceptor degeneration through glial-neuronal interaction.Cell death & disease · 2026Article
- Attenuation of Oxygen-Induced Neovascularization and Inflammation by Neutralizing VEGFA and/or ANG-2 With an Antibody.Genes to cells : devoted to molecular & cellular mechanisms · 2026Article
- Stem cells ameliorate neurotrauma-induced visual disturbances and retinal degeneration via broad normalization of β-catenin-related signaling.International journal of medical sciences · 2026Article
- Sphingosine-1-Phosphate Signaling through Müller Glia Regulates Neuroprotection, Accumulation of Immune Cells, and Neuronal Regeneration in the Rodent Retina.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- The novel antidiabetic medications on diabetic retinopathy: relevant molecular mechanisms, advancing diagnostic innovations, and therapeutic implications.Frontiers in medicine · 2025Review
- The controversial role of nutraceuticals vs. drugs in proliferative retinopathies.Frontiers in neuroscience · 2025Review
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
VEGF is not only the most potent angiogenic factor, but also an important neurotrophic factor. In this study, vitreous expression of six neurotrophic factors were examined in proliferative diabetic retinopathy (PDR) patients with prior anti-VEGF therapy (n = 48) or without anti-VEGF treatment (n = 41) via ELISA. Potential source, variation and impact of these factors were further investigated in a mouse model of oxygen-induced retinopathy (OIR), as well as primary Müller cells and 661W photoreceptor cell line under hypoxic condition. Results showed that vitreous levels of NGF, NT-3, NT-4, BDNF, GDNF and CNTF were significantly higher in eyes undergoing anti-VEGF therapy compared with PDR controls. Statistical correlation between vitreous VEGF and each trophic factor was found. Hypoxia significantly induced the expressions of these neurotrophic factors, whereas application of anti-VEGF agent in OIR model could further upregulate retinal NGF, NT-3, NT-4, together with downregulation of BDNF, GDNF, CNTF, especially in Müller glia. Inhibition of Müller cell-derived VEGF would result in similar neurotrophic changes under hypoxia. With changes of corresponding neurotrophic receptors in the cocultured photoreceptor cells, their synergic effect could protect hypoxic photoreceptor from apoptosis when VEGF inhibition was present. These findings demonstrated that regulation of Müller cell-derived neurotrophic factors might be one of the possible mechanisms by which anti-VEGF therapy produced neuroprotective effects on PDR. These results provided new evidence for the therapeutic strategy of PDR.
Indexed as
Identifiers
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.