ArticleIndian journal of ophthalmology2026
Corneal stromal stem cell-derived extracellular vesicles inhibit corneal neovascularization.
Article in Indian journal of ophthalmology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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
3 citing papers in PubMed.
- M1-primed human corneal stromal stem cell-derived exosomes delivering protein-coding transforming growth factor-β3 RNA promote corneal regeneration.Stem cells translational medicine · 2026Article
- The Role of Epigenetics in Corneal Fibrosis.Epigenomes · 2026Review
- Human Corneal Stromal Stem Cell Treatment Reduces Established Opacities in Chronic Corneal Scarring.Cells · 2026Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
purposeCorneal neovascularization (CNV) threatens corneal transparency and is a leading cause of vision loss. This study evaluates the anti-angiogenic effects of extracellular vesicles (EVs) derived from human corneal stromal stem cells (CSSCs).
methodsCultured human umbilical vein endothelial cells (HUVECs) were treated with CSSC-EVs to examine the influence on cell growth and modulation of angiogenesis using xCELLigence and tube formation assays. In vivo, a mouse model of CNV was induced by silver nitrate (AgNO₃) cauterization, and the injured corneas were treated with CSSC-EV eye drops twice daily for four days. On day 10, new vessel formation on mouse corneas was graded, and the expression of angiogenic markers was assessed using immunostaining and qPCR. Results were analyzed using one-way ANOVA.
resultsHUVEC cultures treated with CSSC-EVs showed reduced growth with a significant increase in cell doubling time. On Geltrex-coated culture surface, HUVECs incubated with CSSC-EVs generated reduced numbers of vascular tube structures, with significantly reduced junctions and nodes. In vivo, CNV developed in AgNO₃-cauterized mouse corneas by day 10 post-injury. Eye drop treatment with CSSC-EVs attenuated the formation of new vessels expressing vascular marker CD31 and lymphatic marker LYVE1. Compared to injured controls treated with phosphate-buffered saline (PBS) eye drops, the expression of angiogenic markers, including ANGPT1 and 2, CD31, VEGFA, VEGFR1, and R2, was significantly downregulated in EV-treated corneas (P < 0.05).
conclusionThe anti-angiogenic effect of CSSC-EVs demonstrated their potential to inhibit CNV. Overall, the topical application of CSSC-EVs was safe and effective for addressing CNV-related pathologies.
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