ArticleCurrent medical science2025
Nintedanib Inhibits VEGF-Induced Neovascularization in Human Conjunctival Vascular Endothelial Cells.
Article in Current medical science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Not yet cited in PubMed.
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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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Corrections and comments
- Erratum issued
Authors and funding
5 authors.
Funding
Abstract
objectiveConjunctival vascularization and fibroblasts are important factors leading to filtering bleb scarring after glaucoma filtering surgery. Previous studies have shown that nintedanib can inhibit the transformation of conjunctival fibroblasts into myofibroblasts, alleviating scar formation. This study aimed to investigate the effect of nintedanib on vascular endothelial growth factor (VEGF)-induced neovascularization of human conjunctival vascular endothelial cells and to reveal the molecular mechanisms involved.
methodsPrimary human conjunctival vascular endothelial cells were cultured with VEGF alone or in combination with nintedanib, and cell proliferation and migration were measured via cell counting kit-8 and scratch assays, respectively. The effect of nintedanib on human conjunctival vascular endothelial cell tube formation was also assayed. The phosphorylation levels of extracellular signal-regulated kinase 1/2 (ERK1/2) and c-Jun N-terminal kinase (JNK) were measured via Western blotting.
resultsVEGF (120 ng/mL) significantly promoted the proliferation of human conjunctival vascular endothelial cells. Nintedanib inhibited the VEGF-induced proliferation of these cells while also suppressing cell migration (P < 0.0001) and vascularization (P < 0.01). Furthermore, nintedanib reduced ERK1/2 (P < 0.01) and JNK phosphorylation (P < 0.001).
conclusionOur study provides new evidence that nintedanib inhibits the proliferation, migration, and neovascularization of human conjunctival vascular endothelial cells and downregulates the expression of p-ERK and p-JNK in the MAPK pathway.
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