ArticleAmerican journal of respiratory cell and molecular biology2023
DOCK2 Promotes Asthma Development by Eliciting Airway Epithelial-Mesenchymal Transition.
Article in American journal of respiratory cell and molecular biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 11 citations in OpenAlex.
- Breaking the bottleneck of asthma treatment: the future of omni-targeted therapy.Journal of advanced research · 2026Review
- Airway epithelial transcriptional response to daily high-dose inhaled corticosteroids in asthma.ERJ open research · 2026Article
- A FoxM1/Smad4 positive feedback loop promotes pancreatic cancer progression.Cell death & disease · 2026Article
- IFITM1 is required for epithelial mesenchymal transition in airway remodeling of allergic asthma.The World Allergy Organization journal · 2026Article
- IL-36 participated in airway remodeling in chronic asthma model by inducing epithelial-mesenchymal transition process.European journal of medical research · 2026Article
- Interpretable Machine Learning Identifies Hub Biomarkers of Renal Fibrosis and Their Potential Medical Applications.Drug design, development and therapy · 2026Article
- High expression of ITGB3 ameliorates asthma by inhibiting epithelial-mesenchymal transformation through suppressing the activation of NF-kB pathway.Scientific reports · 2025Article
- M2 macrophage-derived exosomes reverse TGF-β1-induced epithelial mesenchymal transformation in BEAS-2B cells via the TGF-βRI/Smad2/3 signaling pathway.European journal of medical research · 2025Article
- Review
- Wnt5a-mediated autophagy contributes to the epithelial-mesenchymal transition of human bronchial epithelial cells during asthma.Molecular medicine (Cambridge, Mass.) · 2024Article
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
Abstract
Epithelial-mesenchymal transition (EMT) contributes to airway remodeling, a predominant feature of asthma. DOCK2 (dedicator of cytokinesis 2) is an innate immune signaling molecule involved in vascular remodeling. However, it is unknown if DOCK2 plays a role in airway remodeling during asthma development. In this study, we found that DOCK2 is highly induced in both normal human bronchial epithelial cells treated with house dust mite (HDM) extract and human asthmatic airway epithelium. DOCK2 is also upregulated by TGF-β1 (transforming growth factor β1) during EMT of human bronchial epithelial cells. Importantly, knockdown of DOCK2 inhibits, and overexpression of DOCK2 promotes, TGF-β1-induced EMT. Consistently, DOCK2 deficiency suppresses the EMT of airway epithelium, attenuates the subepithelial fibrosis, and improves pulmonary function in HDM-induced asthmatic lungs. These data suggest that DOCK2 plays an important role in EMT and asthma development. Mechanistically, DOCK2 interacts with transcription factor FoxM1 (forkhead box M1), which enhances FoxM1 binding to mesenchymal marker gene promoters and further promotes mesenchymal marker gene transcription and expression, leading to EMT. Taken together, our study identifies DOCK2 as a novel regulator for airway EMT in an HDM-induced asthma model, thus providing a potential therapeutic target for treatment of asthma.
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