ArticleInternational journal of ophthalmology2025
Nintedanib regulates miR-23b-3p/TGFBR2 axis and competitively binds to TGFBR2 protein, inhibiting EMT process in human pterygium cells.
Article in International journal of ophthalmology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Genome-Wide Association Study of Pterygium Versus Pinguecula Identifies Loci Associated with Lesion-Type Divergence.Ophthalmology science · 2026Article
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Authors and funding
6 authors.
Funding
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Abstract
aimTo investigate the effects of nintedanib on epithelial-mesenchymal transition (EMT) in cells derived from pterygium, aiming to explore its potential as a pharmacological intervention for pterygium treatment.
methodsPrimary human pterygium epithelial cells (hPEC) and human conjunctival epithelial (hCJE) cells were isolated from patients, cultured, and characterized. The impact of nintedanib on transforming growth factor beta (TGF-β)-induced EMT was assessed by examining the expression of EMT markers such as vimentin and E-cadherin. Additionally, the modulation of the miR-23b-3p/transforming growth factor beta receptor 2 (TGFBR2)/Smad2 pathway by nintedanib was investigated to elucidate its potential antifibrotic mechanism.
resultsThe expression of miR-23b-3p gene in hCJE cells was significantly higher than that in hPEC cells. Nintedanib effectively mitigated TGF-β-induced EMT in cells derived from pterygium, as evidenced by the downregulation of vimentin and upregulation of E-cadherin. When the nintedanib concentration exceeded 1 µmol/L, it significantly suppressed the proliferation of hPEC cells and significantly inhibited the migration distance of hPEC cells within 48h (
conclusionNintedanib is found to modulate the miR-23b-3p/TGFBR2/Smad2 pathway, suggesting a novel antifibrotic mechanism. These findings collectively highlight nintedanib's therapeutic potential in managing pterygium, marking a significant step toward non-surgical treatment options. Nintedanib may offer a targeted pharmacological treatment that could complement or reduce the need for surgical interventions.
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