ArticlePloS one2025
Plasma-activated media inhibits epithelial-mesenchymal transition and ameliorates intestinal fibrosis through the PPARγ/TGF-β1/SMAD3 pathway.
Article in PloS one, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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
1 citing paper in PubMed.
- MMT: A Potential Mechanism of Myocardial Fibrosis - Regulation of the TGF-β1/Smad3 Pathway and Prospects for Targeted Therapy.Reviews in cardiovascular medicine · 2026Review
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammatory bowel disease often complicates intestinal lumen stenosis, and intestinal fibrosis is the core pathological process leading to its development. Currently, there are no effective drug treatments available to prevent or improve intestinal fibrosis. Previous studies have shown that PAM (plasma-activated media) inhibits epithelial-mesenchymal transition (EMT) and improves skin fibrosis by regulating the PPARγ/TGF-β1 axis. However, it is unclear whether PAM can improve intestinal fibrosis. We used a gradient concentration of PAM to intervene in the dextran sulfate sodium (DSS)-induced mouse intestinal fibrosis model to evaluate its effects onalleviating fibrosis and explore the specific molecular mechanisms. In addition, we used PAM to intervene in the TGF-β1-induced rat intestinal crypt epithelial cell (IEC-6) EMT and fibrosis in an in vitro model to further explore the molecular mechanisms by which PAM improves intestinal fibrosis. We found that PAM can improve intestinal fibrosis by inhibiting epithelial-mesenchymal transition through the PPARγ/TGF-β1/SMAD signaling pathway.
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