ArticleAmerican journal of physiology. Cell physiology2022
DOCK2 contributes to pulmonary fibrosis by promoting lung fibroblast to myofibroblast transition.
Article in American journal of physiology. Cell physiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 20 citations in OpenAlex.
- Geranylgeranylacetone Alleviates Pulmonary Fibrosis in Mice by Activation of Nrf2 /HO-1/NQO1 Pathway.Cell biochemistry and biophysics · 2026Article
- Interpretable Machine Learning Identifies Hub Biomarkers of Renal Fibrosis and Their Potential Medical Applications.Drug design, development and therapy · 2026Article
- Inhibition of RAC1 activator DOCK2 ameliorates cholestatic liver injury via regulating macrophage polarisation and hepatic stellate cell activation.Biology direct · 2025Article
- Novel insights into the ROCK-JAK-STAT signaling pathway in upper respiratory tract infections and neurodegenerative diseases.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- M2 Macrophage and Extracellular Matrix Genes Are Enriched in High-Activity Lichen Planopilaris.Dermatology research and practice · 2025Article
- Article
- 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
- Article
- DOCK2 Promotes Atherosclerosis by Mediating the Endothelial Cell Inflammatory Response.The American journal of pathology · 2024Article
- MARCH8 downregulation modulates profibrotic responses including myofibroblast differentiation.American journal of physiology. Cell physiology · 2023Article
- Etiology and Pathogenesis of Rheumatoid Arthritis-Interstitial Lung Disease.International journal of molecular sciences · 2023Review
- Linking Adiposity to Interstitial Lung Disease: The Role of the Dysfunctional Adipocyte and Inflammation.Cells · 2023Review
- Wilms Tumor 1-Driven Fibroblast Activation and Subpleural Thickening in Idiopathic Pulmonary Fibrosis.International journal of molecular sciences · 2023Review
- Construction of a neural network diagnostic model for renal fibrosis and investigation of immune infiltration characteristics.Frontiers in immunology · 2023Article
- Multiomic analysis reveals conservation of cancer-associated fibroblast phenotypes across species and tissue of origin.Cancer cell · 2022Article
- Insights from DOCK2 in cell function and pathophysiology.Frontiers in molecular biosciences · 2022Review
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Idiopathic pulmonary fibrosis (IPF) is the most common chronic interstitial lung disease and is characterized by progressive scarring of the lung. Transforming growth factor-β (TGF-β) signaling plays an essential role in IPF and drives fibroblast to myofibroblast transition (FMT). Dedicator of cytokinesis 2 (DOCK2) is known to regulate diverse immune functions by activating Rac and has been recently implicated in pleural fibrosis. We now report a novel role of DOCK2 in pulmonary fibrosis development by mediating FMT. In primary normal and IPF human lung fibroblasts (HLFs), TGF-β induced DOCK2 expression concurrent with FMT markers, smooth muscle α-actin (α-SMA), collagen-1, and fibronectin. Knockdown of DOCK2 significantly attenuated TGF-β-induced expression of these FMT markers. In addition, we found that the upregulation of DOCK2 by TGF-β is dependent on both Smad3 and ERK pathways as their respective inhibitors blocked TGF-β-mediated induction. TGF-β also stabilized DOCK2 protein, which contributes to increased DOCK2 expression. In addition, DOCK2 was also dramatically induced in the lungs of patients with IPF and in bleomycin, and TGF-β induced pulmonary fibrosis in C57BL/6 mice. Furthermore, increased lung DOCK2 expression colocalized with the FMT marker α-SMA in the bleomycin-induced pulmonary fibrosis model, implicating DOCK2 in the regulation of lung fibroblast phenotypic changes. Importantly, DOCK2 deficiency also attenuated bleomycin-induced pulmonary fibrosis and α-SMA expression. Taken together, our study demonstrates a novel role of DOCK2 in pulmonary fibrosis by modulating FMT and suggests that targeting DOCK2 may present a potential therapeutic strategy for the prevention or treatment of IPF.
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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.