ArticleMolecular therapy. Nucleic acids2019
MicroRNA-29b Mediates Lung Mesenchymal-Epithelial Transition and Prevents Lung Fibrosis in the Silicosis Model.
Article in Molecular therapy. Nucleic acids, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.
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Who cites it
33 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The Immunological Microenvironment and the Emerging Role of Stem Cells Therapy in Peyronie's Disease: A Systematic Narrative Review.International journal of molecular sciences · 2023Pooled it
- miR-29b as an Anti-Fibrotic Therapeutic: Mechanisms, Disease Biology and Translational Opportunities.Cells · 2026Review
- MicroRNAs as Mediators of Mechanotransduction: from Fundamental Mechanisms to Therapeutic Applications.Cell biochemistry and biophysics · 2026Review
- Review
- Silencing miR-1291-LEFTY2 axis diminishes the myofibroblast activities and reactive oxygen species generation of fibrotic buccal mucosal fibroblasts.Journal of dental sciences · 2025Article
- Long non-coding RNA H19 mediates the miR-29b/transforming growth factor-β1/Drosophila mothers against decapentaplegic 3 signalling pathway to promote bladder fibrosis in diabetic rats.International urology and nephrology · 2024Article
- A comprehensive retrospect on the current perspectives and future prospects of pneumoconiosis.Frontiers in public health · 2024Review
- microRNA-141-3p mediates epithelial cell proliferation, apoptosis, and epithelial-mesenchymal transition and alleviates pulmonary fibrosis in mice via Spred2.Histology and histopathology · 2023Article
- Animal models of silicosis: fishing for new therapeutic targets and treatments.European respiratory review : an official journal of the European Respiratory Society · 2023Review
- MiR-148a-3p within HucMSC-Derived Extracellular Vesicles Suppresses Hsp90b1 to Prevent Fibroblast Collagen Synthesis and Secretion in Silica-Induced Pulmonary Fibrosis.International journal of molecular sciences · 2023Article
- Single-cell transcriptome sequencing-based analysis: probing the mechanisms of glycoprotein NMB regulation of epithelial cells involved in silicosis.Particle and fibre toxicology · 2023Article
- Dulaglutide Ameliorates Intrauterine Adhesion by Suppressing Inflammation and Epithelial-Mesenchymal Transition via Inhibiting the TGF-β/Smad2 Signaling Pathway.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Preclinical Mouse Model of Silicosis.Methods in molecular biology (Clifton, N.J.) · 2023Article
- The emerging role of epigenetic regulation in the progression of silicosis.Clinical epigenetics · 2022Review
- The Role of miR-29s in Human Cancers-An Update.Biomedicines · 2022Review
- Current and prospective applications of exosomal microRNAs in pulmonary fibrosis (Review).International journal of molecular medicine · 2022Review
- Epigenetic Changes and Functions in Pneumoconiosis.Oxidative medicine and cellular longevity · 2022Review
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Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lung epithelial-mesenchymal transition (EMT) plays an important role in silicosis fibrosis. The reverse process of EMT is mesenchymal-epithelial transition (MET), which is viewed as an anti-EMT therapy and is a good target toward fibrosis. MicroRNAs (miRNAs) have emerged as potent regulators of EMT and MET programs, and, hence, we tested the miRNA expression using microarray assay and investigated their roles in silica-induced EMT in lung epithelial cells. We found that miRNA-29b (miR-29b) was dynamically downregulated by silica and influenced the promotion of MET in RLE-6TN cells. Furthermore, delivery of miR-29b to mice significantly inhibited silica-induced EMT, prevented lung fibrosis, and improved lung function. Together, our results clearly demonstrated that miR-29b acted as a novel negative regulator of silicosis fibrosis-inhibited lung fibrosis, probably by promoting MET and by suppressing EMT in the lung. These findings may represent a new potential therapeutic target for treating silicosis fibrosis.
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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 OpenQuestion graph.