ArticleNature communications2025
The CCL20-integrin α5β1 interaction enhances TGF-β/Smad signaling to promote fibroblast activation in pulmonary fibrosis.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed.
- Clearing the Pulmonary Traffic Jam With Dual-Enzyme Inhalable Nanoparticles Restore Airflow and Reverse Fibrotic Remodeling.Advanced healthcare materials · 2026Article
- Article
- Tumor-derived CCL20 activates tumor-associated neutrophils, predicting good prognosis in endometrial cancer.Translational cancer research · 2026Article
- Epithelial Integrins Coordinate Cellular Crosstalk Through the Regulation of Cytokines During Tissue Remodeling.International journal of molecular sciences · 2026Review
- Direct Extracellular Matrix Modulation Attenuates Intestinal Fibrosis via a Fibronectin-Targeted Approach.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Recent advances in biomarkers for cardiac fibrosis.Frontiers in cardiovascular medicine · 2026Review
- Bridging the gaps: the gut-lung axis and microbial metabolites in the pathogenesis and treatment of pulmonary fibrosis.Frontiers in medicine · 2026Review
Corrections and comments
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Authors and funding
17 authors.
Funding
Abstract
Limited therapeutic options are available for pulmonary fibrosis because its molecular pathogenesis remains unclear. Here, we find that chemokine CCL20 expression is increased in both murine models and patients with pulmonary fibrosis. Type 2 alveolar epithelial cells are identified as the major producers of CCL20, and increased CCL20 expression results from decreased expression of the transcription factor JUN. AEC2-specific deletion of CCL20 protects mice from bleomycin-induced pulmonary fibrosis. Mechanistic studies reveal that CCL20 interacts with integrin α5β1, but not the classical receptor CCR6, on fibroblasts and subsequently enhances TGF-β/Smad signaling, which promotes the differentiation of lung fibroblasts into myofibroblasts. Antibody blockade of CCL20 or disruption of the CCL20-integrin α5β1 interaction attenuates established pulmonary fibrosis. Overall, our study highlights the CCL20-integrin α5β1-TGF-β signaling cascade as a potential therapeutic target for pulmonary fibrosis.
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Registered trials
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