ArticleJournal of cellular and molecular medicine2020
miR-34a-5p Attenuates EMT through targeting SMAD4 in silica-induced pulmonary fibrosis.
Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 42 citations in OpenAlex.
- The emerging roles of microRNAs in pneumoconiosis: pathogenic mechanisms and clinical implications.Frontiers in cell and developmental biology · 2026Review
- Circular RNA hsa_circ_0000118 promotes atrial fibrosis by regulating the microRNA‑34a‑5p/Smad4 axis.Molecular medicine reports · 2025Article
- Shared and Context-Specific Mechanisms of EMT and Cellular Plasticity in Cancer and Fibrotic Diseases.International journal of molecular sciences · 2025Review
- Effect of pirfenidone on pulmonary fibrosis in acute lung injury via the regulation of the miR-34a-5p/TGF-β1/SMAD pathway.Journal of thoracic disease · 2025Article
- Bicyclol attenuates pulmonary fibrosis with silicosis via both canonical and non-canonical TGF-β1 signaling pathways.Journal of translational medicine · 2024Article
- MicroRNA-452-5p regulates fibrogenesis via targeting TGF-β/SMAD4 axis in SCN5A-knockdown human cardiac fibroblasts.iScience · 2024Article
- Revisiting the role of MicroRNAs in the pathogenesis of idiopathic pulmonary fibrosis.Frontiers in cell and developmental biology · 2024Review
- Advances in the Study of Non-Coding RNA in the Signaling Pathway of Pulmonary Fibrosis.International journal of general medicine · 2024Review
- NLRP3 Inflammasome Mediates Silica-induced Lung Epithelial Injury and Aberrant Regeneration in Lung Stem/Progenitor Cell-derived Organotypic Models.International journal of biological sciences · 2023Article
- Inhibition of Oncogenic Src Ameliorates Silica-Induced Pulmonary Fibrosis via PI3K/AKT Pathway.International journal of molecular sciences · 2023Article
- The emerging role of epigenetic regulation in the progression of silicosis.Clinical epigenetics · 2022Review
- Current and prospective applications of exosomal microRNAs in pulmonary fibrosis (Review).International journal of molecular medicine · 2022Review
- Multiple roles of mothers against decapentaplegic homolog 4 in tumorigenesis, stem cells, drug resistance, and cancer therapy.World journal of stem cells · 2022Review
- MicroRNA-34a: A Novel Therapeutic Target in Fibrosis.Frontiers in physiology · 2022Review
- CAV2 Regulates Mir-4723/Wnt7A Signalling Axis through Endocytosis and Epithelial-Mesenchymal Transition to Promote Proliferation, Invasion, and Metastasis of Pancreatic Cancer Cells.Journal of Cancer · 2022Article
- Epigenetic Changes and Functions in Pneumoconiosis.Oxidative medicine and cellular longevity · 2022Review
- Herbal compounds in the treatment of pulmonary silicosis.Physiological research · 2021Review
- Pulmonary fibrosis from molecular mechanisms to therapeutic interventions: lessons from post-COVID-19 patients.Biochemical pharmacology · 2021Review
- Mesenchymal stem cells ameliorate silica-induced pulmonary fibrosis by inhibition of inflammation and epithelial-mesenchymal transition.Journal of cellular and molecular medicine · 2021Article
- New Insights into Pathomechanisms and Treatment Possibilities for Lung Silicosis.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Silicosis is an incurable occupational disease, and its pathological feature is diffuse pulmonary fibrosis. Pulmonary epithelial-mesenchymal transition (EMT) is one of the important events in the pathogenesis of silicosis. Previous studies found that abnormal expression of various microRNAs (miRNAs) involved in the development of lung fibrosis. However, their roles in silicosis have not been elucidated. To research the biological effects of miR-34a in EMT process in silica-induced lung fibrosis, we established the silicosis model in mouse and miR-34a intervention in a cell model of TGF-β1 stimulated lung epithelial cells (A549). The results showed that miR-34a expression was down-regulated in the fibrotic lung tissue after silica treatment, and it was similarly expressed in A549 cells stimulated by TGF-β1. Meanwhile, silica-induced EMT process can increase expression of two mesenchymal markers, α-SMA and vimentin. Furthermore, overexpression miR-34a markedly inhibited EMT stimulated by TGF-β1. Mechanistically, SMAD4 was identified as the target of miR-34a. SMAD4 levels decreased in mRNA and protein levels in A549 cells upon miR-34a overexpression. In addition, the knockdown of SMAD4 blocked the EMT process. Taken together, miR-34a regulated EMT, which might be partially realized by targeting SMAD4. Our data might provide new insight into treatment targets for silica-induced pulmonary fibrosis.
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