ArticleJournal of translational medicine2024
MiR-146a reduces fibrosis after glaucoma filtration surgery in rats.
Article in Journal of translational medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Adipose-Derived Mesenchymal Stem Cell Exosome miR-146a-5p Attenuates TGF-β2-Induced Transformation of Human Tenon's Capsule Fibroblasts by Targeting SMAD4.Investigative ophthalmology & visual science · 2026Article
- LncRNA ANRIL inhibits TGF-β1-induced proliferation, migration, and fibrosis of Tenon's capsule fibroblasts from glaucoma patients by reducing IL-22-RA1 stability and expression.International ophthalmology · 2026Article
- Targeting CRBN With Thalidomide Suppresses Fibrosis After Glaucoma Drainage Surgery Through NF-κB Pathway Inhibition.Investigative ophthalmology & visual science · 2026Article
- Bladder Defect Repair by Polycaprolactone/Gelatin Nanofiber Scaffolds Loaded with Mitomycin Through Anti-Fibrotic Effects.International journal of nanomedicine · 2026Article
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Authors and funding
8 authors.
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Abstract
purposeTo explore the impact of microRNA 146a (miR-146a) and the underlying mechanisms in profibrotic changes following glaucoma filtering surgery (GFS) in rats and stimulation by transforming growth factor (TGF)-β1 in rat Tenon's capsule fibroblasts.
methodsCultured rat Tenon's capsule fibroblasts were treated with TGF-β1 and analyzed with microarrays for mRNA profiling to validate miR-146a as the target. The Tenon's capsule fibroblasts were then respectively treated with lentivirus-mediated transfection of miR-146a mimic or inhibitor following TGF-β1 stimulation in vitro, while GFS was performed in rat eyes with respective intraoperative administration of miR-146a, mitomycin C (MMC), or 5-fluorouracil (5-FU) in vivo. Profibrotic genes expression levels (fibronectin, collagen Iα, NF-KB, IL-1β, TNF-α, SMAD4, and α-smooth muscle actin) were determined through qPCR, Western blotting, immunofluorescence staining and/or histochemical analysis in vitro and in vivo. SMAD4 targeting siRNA was further used to treat the fibroblasts in combination with miR-146a intervention to confirm its role in underlying mechanisms.
resultsUpregulation of miR-146a reduced the proliferation rate and profibrotic changes of rat Tenon's capsule fibroblasts induced by TGF-β1 in vitro, and mitigated subconjunctival fibrosis to extend filtering blebs survival after GFS in vivo, where miR-146a decreased expression levels of NF-KB-SMAD4-related genes, such as fibronectin, collagen Iα, NF-KB, IL-1β, TNF-α, SMAD4, and α-smooth muscle actin(α-SMA). Additionally, SMAD4 is a key target gene in the process of miR-146a inhibiting fibrosis.
conclusionsMiR-146a effectively reduced TGF-β1-induced fibrosis in rat Tenon's capsule fibroblasts in vitro and in vivo, potentially through the NF-KB-SMAD4 signaling pathway. MiR-146a shows promise as a novel therapeutic target for preventing fibrosis and improving the success rate of GFS.
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