ArticleParticle and fibre toxicology2020
Particulate matters increase epithelial-mesenchymal transition and lung fibrosis through the ETS-1/NF-κB-dependent pathway in lung epithelial cells.
Article in Particle and fibre toxicology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 50 citations in OpenAlex.
- Preliminary outcomes and transcriptomic analysis of xenogeneic human-derived acellular dermal matrix patches for complex ureteral stricture reconstruction in a porcine model.Translational andrology and urology · 2026Article
- Epithelial-to-mesenchymal transition as a central driver of tumor cell plasticity.Nature cancer · 2026Review
- Direct Extracellular Matrix Modulation Attenuates Intestinal Fibrosis via a Fibronectin-Targeted Approach.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Polystyrene nanoplastics-induced lung epithelial cells ferroptosis promotes pulmonary fibrosis via YY1/FTL axis.Materials today. Bio · 2026Article
- Prognostic risk model based on cholesterol metabolism-Associated gene module for idiopathic pulmonary fibrosis.PloS one · 2026Article
- Development of a three-dimensional airway organoid-pillar dish (3D AO-PD) platform for particulate matter-induced airway toxicity analysis.Materials today. Bio · 2025Article
- The CCL20-integrin α5β1 interaction enhances TGF-β/Smad signaling to promote fibroblast activation in pulmonary fibrosis.Nature communications · 2025Article
- Beyond the pill: incrimination of nuclear factor-kappa B and their targeted phytomedicine for pulmonary fibrosis.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Air pollution and alveolar health.European respiratory review : an official journal of the European Respiratory Society · 2025Review
- Integrins and pulmonary fibrosis: Pathogenic roles and therapeutic opportunities.Biomolecules & biomedicine · 2025Review
- Exosomal miR-499a-5p from human umbilical cord mesenchymal stem cells attenuates liver fibrosis via targeting ETS1/GPX4-mediated ferroptosis in hepatic stellate cells.Journal of nanobiotechnology · 2025Article
- Club cell secretory protein 16 promotes cell proliferation and inhibits inflammation and pyroptosis in response to particulate matter 2.5-induced epithelial damage in asthmatic mice.Journal of thoracic disease · 2025Article
- Zinc Iodide Dimethyl Sulfoxide Reduces Collagen Deposition by Increased Matrix Metalloproteinase-2 Expression and Activity in Lung Fibroblasts.Biomedicines · 2024Article
- Prolyl oligopeptidase inhibition ameliorates experimental pulmonary fibrosis both in vivo and in vitro.Respiratory research · 2023Article
- The Role of miRNA in Renal Fibrosis Leading to Chronic Kidney Disease.Biomedicines · 2023Review
- Integrated genomics approaches identify transcriptional mediators and epigenetic responses to Afghan desert particulate matter in small airway epithelial cells.Physiological genomics · 2022Article
- Article
- Exosomes derived from mesenchymal stem cells ameliorate renal fibrosis via delivery of miR-186-5p.Human cell · 2022Article
- Metformin attenuates silica-induced pulmonary fibrosis via AMPK signaling.Journal of translational medicine · 2021Article
- Upregulation of ACE2 and TMPRSS2 by particulate matter and idiopathic pulmonary fibrosis: a potential role in severe COVID-19.Particle and fibre toxicology · 2021Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundParticulate matters (PMs) in ambient air pollution are closely related to the incidence of respiratory diseases and decreased lung function. Our previous report demonstrated that PMs-induced oxidative stress increased the expression of proinflammatory intracellular adhesion molecule-1 (ICAM-1) through the IL-6/AKT/STAT3/NF-κB pathway in A549 cells. However, the role of O-PMs in epithelial-mesenchymal transition (EMT) development and pulmonary fibrosis and the related mechanisms have not been determined. The aim of this study was to investigate the effects of O-PMs on the pathogenesis of EMT and pulmonary fibrosis as well as the expression of ETS-1 and NF-κB p65, in vitro and in vivo.
resultsO-PMs treatment induced EMT development, fibronectin expression, and cell migration. O-PMs affected the expression of the EMT-related transcription factors NF-κB p65 and ETS-1. Interference with NF-κB p65 significantly decreased O-PMs-induced fibronectin expression. In addition, O-PMs affected the expression of fibronectin, E-cadherin, and vimentin through modulating ETS-1 expression. ATN-161, an antagonist of integrin α5β1, decreased the expression of fibronectin and ETS-1 and EMT development. EMT development and the expression of fibronectin and ETS-1 were increased in the lung tissue of mice after exposure to PMs for 7 and 14 days. There was a significant correlation between fibronectin and ETS-1 expression in human pulmonary fibrosis tissue.
conclusionO-PMs can induce EMT and fibronectin expression through the activation of transcription factors ETS-1 and NF-κB in A549 cells. PMs can induce EMT development and the expression of fibronectin and ETS-1 in mouse lung tissues. These findings suggest that the ETS-1 pathway could be a novel and alternative mechanism for EMT development and pulmonary fibrosis.
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