ArticleJournal of dental sciences2026
Metformin alleviates the progression of oral submucous fibrosis through downregulation of metastasis associated lung adenocarcinoma transcript 1 (MALAT1).
Article in Journal of dental sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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
1 citing paper in PubMed.
- Fibrotic-Angiogenic Signaling Networks in Oral Submucous Fibrosis: Pathobiology and Therapeutic Targeting.International journal of molecular sciences · 2026Review
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Materials and methods: The cytotoxic effects of metformin on normal and fibrotic buccal mucosal fibroblasts (fBMFs) derived from OSF tissues were evaluated using the MTT assay. Collagen gel contraction, wound healing, and transwell migration assays were carried out to assess myofibroblast features. In addition, the expression levels of alpha-1 type I collagen (COL1A1), alpha-smooth muscle actin (α-SMA) and Smad2 were measured. Moreover, RNA sequencing was performed to explore potential targets participating in the anti-fibrotic effects of metformin. Results: A lower dose of metformin was sufficient to inhibit the proliferation of fBMFs without affecting normal BMFs, and to attenuate various myofibroblast characteristics, including collagen gel contraction, wound healing, transwell migration capacities, and the expression of fibrosis markers. Additionally, we showed that administration of metformin prevented the arecoline-induced myofibroblast activation. Most importantly, our results suggest that metformin may exert suppressive effects on myofibroblast activities by inhibiting ROS accumulation through the downregulation of MALAT1. Conclusion: These findings indicate that metformin may serve as a preventive agent against OSF progression.
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Registered trials
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