ArticleJournal of dental sciences2025
Silencing miR-1291-LEFTY2 axis diminishes the myofibroblast activities and reactive oxygen species generation of fibrotic buccal mucosal fibroblasts.
Article in Journal of dental sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background/purpose: Oral submucous fibrosis (OSF) is a potentially malignant disorder characterized by chronic inflammation and excessive collagen deposition, leading to fibrosis in the oral mucosa. This study aimed to explore the contribution of the miR-1291/LEFTY2 axis in the development of OSF progression. Materials and methods: Expression of miR-1291 was evaluated in OSF tissues and primary myofibroblasts using RNA sequencing and qRT-PCR. The functional role of miR-1291 and LEFTY2 were investigated using miR-1291 inhibitor and lentiviral-mediated overexpression of LEFTY2, respectively. A luciferase reporter assay was conducted to examine the direct interaction between miR-1291 and LEFTY2. Myofibroblast activities were assessed by collagen gel contraction, wound healing, and transwell migration assays. Reactive oxygen species (ROS) production was measured by flow cytometry. Results: MiR-1291 was markedly upregulated in OSF tissues and myofibroblasts, and it was positively correlated with a couple of fibrosis markers, including α-SMA and TGF-β1. Inhibition of miR-1291 suppressed myofibroblast activities and ROS generation. Luciferase reporter assays confirmed that miR-1291 is directly bound to the three prime untranslated region (3'UTR) of LEFTY2, a negative regulator of TGF-β signaling. Overexpression of LEFTY2 attenuated phosphorylation of Smad, myofibroblast activities, and ROS production. Conclusion: Our findings demonstrated that miR-1291 may promote fibrosis in OSF by suppressing LEFTY2 expression to increase myofibroblast activation via regulation of ROS accumulation and TGF-β/Smad signaling.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.