ArticleAmerican journal of respiratory cell and molecular biology2022
DOCK2 Promotes Pleural Fibrosis by Modulating Mesothelial to Mesenchymal Transition.
Article in American journal of respiratory cell and molecular biology, 2022. 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, 25 citations in OpenAlex.
- Sprayable asymmetric hydrogel prevents postoperative pleural adhesions via physical and biological dual therapy.Materials today. Bio · 2026Article
- Interpretable Machine Learning Identifies Hub Biomarkers of Renal Fibrosis and Their Potential Medical Applications.Drug design, development and therapy · 2026Article
- A mesothelial differentiation gateway drives fibrosis.Nature communications · 2025Article
- The Role of Tuftelin-1 in Mesomesenchymal Transition of Pleural Mesothelial Cells and the Progression of Pleural Fibrosis.American journal of respiratory cell and molecular biology · 2025Article
- BRD4 Mediates Transforming Growth Factor-β-Induced Smooth Muscle Cell Differentiation from Mesenchymal Progenitor Cells.International journal of molecular sciences · 2025Article
- Perspective and update: intrapleural fibrinolytic therapy for pleural infections and other forms of pleural organization.Respiratory research · 2025Review
- Inhibition of RAC1 activator DOCK2 ameliorates cholestatic liver injury via regulating macrophage polarisation and hepatic stellate cell activation.Biology direct · 2025Article
- Epithelial-to-mesenchymal transition is an active process in the large airways of patients with asthma-COPD overlap and partially abrogated by inhaled corticosteroid treatment: a bronchoscopy endobronchial biopsy study.Frontiers in immunology · 2025Article
- Silencing DOCK2 Attenuates Cardiac Fibrosis Following Myocardial Infarction in Mice Via Targeting PI3K/Akt and Wnt/β-Catenin Pathways.Journal of cardiovascular translational research · 2024Article
- DOCK2 Promotes Atherosclerosis by Mediating the Endothelial Cell Inflammatory Response.The American journal of pathology · 2024Article
- Role of ZIP kinase in development of myofibroblast differentiation from HPMCs.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- The mTORC2/SGK1/NDRG1 Signaling Axis Is Critical for the Mesomesenchymal Transition of Pleural Mesothelial Cells and the Progression of Pleural Fibrosis.American journal of respiratory cell and molecular biology · 2024Article
- MARCH8 downregulation modulates profibrotic responses including myofibroblast differentiation.American journal of physiology. Cell physiology · 2023Article
- DOCK2 Promotes Asthma Development by Eliciting Airway Epithelial-Mesenchymal Transition.American journal of respiratory cell and molecular biology · 2023Article
- Characterization of the pleural microenvironment niche and cancer transition using single-cell RNA sequencing in EGFR-mutated lung cancer.Theranostics · 2023Article
- Extra-hematopoietic immunomodulatory role of the guanine-exchange factor DOCK2.Communications biology · 2022Article
- DOCK2 contributes to pulmonary fibrosis by promoting lung fibroblast to myofibroblast transition.American journal of physiology. Cell physiology · 2022Article
- DOCK-t(w)o Pleural Fibrosis.American journal of respiratory cell and molecular biology · 2022Article
- Update on Novel Targeted Therapy for Pleural Organization and Fibrosis.International journal of molecular sciences · 2022Review
- Insights from DOCK2 in cell function and pathophysiology.Frontiers in molecular biosciences · 2022Review
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9 authors at 1 institution in 1 country.
Funding
Abstract
Mesothelial to mesenchymal transition (MesoMT) is one of the crucial mechanisms underlying pleural fibrosis, which results in restrictive lung disease. DOCK2 (dedicator of cytokinesis 2) plays important roles in immune functions; however, its role in pleural fibrosis, particularly MesoMT, remains unknown. We found that amounts of DOCK2 and the MesoMT marker α-SMA (α-smooth muscle actin) were significantly elevated and colocalized in the thickened pleura of patients with nonspecific pleuritis, suggesting the involvement of DOCK2 in the pathogenesis of MesoMT and pleural fibrosis. Likewise, data from three different pleural fibrosis models (TGF-β [transforming growth factor-β], carbon black/bleomycin, and streptococcal empyema) consistently demonstrated DOCK2 upregulation and its colocalization with α-SMA in the pleura. In addition, induced DOCK2 colocalized with the mesothelial marker calretinin, implicating DOCK2 in the regulation of MesoMT. Our
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