ArticleRespiratory research2017
Anti-fibrotic efficacy of nintedanib in pulmonary fibrosis via the inhibition of fibrocyte activity.
Article in Respiratory research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 2 of them syntheses that pooled it.
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Who cites it
50 citing papers in PubMed, 2 syntheses or guidelines pooled it, 105 citations in OpenAlex.
- Pulmonary fibrosis complicated by lung cancer: bibliometric analysis from 2004 to 2024 - research status, trends and future directions.Frontiers in immunology · 2025Pooled it
- Extended Exhaled Nitric Oxide Analysis in Interstitial Lung Diseases: A Systematic Review.International journal of molecular sciences · 2020Pooled it
- In Vitro Assessment of Nintedanib in Keratoconus Corneal Stromal Microenvironment.Biomolecules · 2026Article
- Article
- Article
- Molecular mechanisms of ovarian fibrosis.Molecular human reproduction · 2026Review
- Nintedanib Enhances the Antibacterial Activity of Bedaquiline Against Non-Tuberculous Mycobacteria: In vitro and in Mice Models.Infection and drug resistance · 2026Article
- Biofabrication of a 3D human skeletal muscle microenvironment to study the early steps of fibrosis.Materials today. Bio · 2025Article
- The Role of Antifibrotic Therapy in Pulmonary Fibrosis and Lung Cancer: A Multicenter Retrospective Analysis.Biomedicines · 2025Article
- Modulating NLRP3 Inflammasomes in Idiopathic Pulmonary Fibrosis: A Comprehensive Review on Flavonoid-Based Interventions.Cell biochemistry and biophysics · 2025Review
- Novel Approaches for the Treatment of Pulmonary Fibrosis with Emphasis on the Role of Galectin-3 Inhibitors as a Potential Therapeutic Approach.Current drug research reviews · 2025Review
- Cytokine Expression Profiling in Idiopathic Pulmonary Fibrosis: Insights From Integrative Proteomic Analysis.Canadian respiratory journal · 2025Article
- Current state of signaling pathways associated with the pathogenesis of idiopathic pulmonary fibrosis.Respiratory research · 2024Review
- Potential Rheumatoid Arthritis-Associated Interstitial Lung Disease Treatment and Computational Approach for Future Drug Development.International journal of molecular sciences · 2024Review
- Single-Cell RNA-Sequencing Identifies Bone Marrow-Derived Progenitor Cells as a Main Source of Extracellular Matrix-Producing Cells Across Multiple Organ-Based Fibrotic Diseases.International journal of biological sciences · 2024Article
- Lung fibrosis in sarcoidosis. Is there a place for antifibrotics?Frontiers in pharmacology · 2024Review
- Perspectives on Post-COVID-19 Pulmonary Fibrosis Treatment.Journal of personalized medicine · 2023Review
- Molecular mechanisms of AMPK/YAP/NLRP3 signaling pathway affecting the occurrence and development of ankylosing spondylitis.Journal of orthopaedic surgery and research · 2023Article
- A systematic review of the research progress of traditional Chinese medicine against pulmonary fibrosis: from a pharmacological perspective.Chinese medicine · 2023Review
- A polo-like kinase inhibitor identified by computational repositioning attenuates pulmonary fibrosis.Respiratory research · 2023Article
Corrections and comments
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Authors and funding
16 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNintedanib, a tyrosine kinase inhibitor that is specific for platelet-derived growth factor receptors (PDGFR), fibroblast growth factor receptors (FGFR), and vascular endothelial growth factor receptors (VEGFR), has recently been approved for idiopathic pulmonary fibrosis. Fibrocytes are bone marrow-derived progenitor cells that produce growth factors and contribute to fibrogenesis in the lungs. However, the effects of nintedanib on the functions of fibrocytes remain unclear.
methodsHuman monocytes were isolated from the peripheral blood of healthy volunteers. The expression of growth factors and their receptors in fibrocytes was analyzed using ELISA and Western blotting. The effects of nintedanib on the ability of fibrocytes to stimulate lung fibroblasts were examined in terms of their proliferation. The direct effects of nintedanib on the differentiation and migration of fibrocytes were also assessed. We investigated whether nintedanib affected the accumulation of fibrocytes in mouse lungs treated with bleomycin.
resultsHuman fibrocytes produced PDGF, FGF2, and VEGF-A. Nintedanib and specific inhibitors for each growth factor receptor significantly inhibited the proliferation of lung fibroblasts stimulated by the supernatant of fibrocytes. Nintedanib inhibited the migration and differentiation of fibrocytes induced by growth factors in vitro. The number of fibrocytes in the bleomycin-induced lung fibrosis model was reduced by the administration of nintedanib, and this was associated with anti-fibrotic effects.
conclusionsThese results support the role of fibrocytes as producers of and responders to growth factors, and suggest that the anti-fibrotic effects of nintedanib are at least partly mediated by suppression of fibrocyte function.
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