ArticleFrontiers in pharmacology2020
Nintedanib Inhibits Wnt3a-Induced Myofibroblast Activation by Suppressing the Src/β-Catenin Pathway.
Article in Frontiers in pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 23 citations in OpenAlex.
- Effects of the WNT signaling pathway on inflammation and fibrosis in idiopathic pulmonary fibrosis: Clinical, radiological and molecular evaluation.Experimental and therapeutic medicine · 2026Article
- [Role and mechanism of Wnt9a in human and mouse chronic wound healing].Zhonghua shao shang yu chuang mian xiu fu za zhi · 2026Article
- Antifibrotics with Cross-Indication Potential: Challenges and Progress Towards a Universal Fibrosis-Modifying Therapy.Drug design, development and therapy · 2026Review
- Understanding the Mechanisms Driving Fibrosis Following Cochlear Implantation-Lessons from Other Tissues.Cells · 2025Review
- Nintedanib preserves lung growth and prevents pulmonary hypertension in a hyperoxia-induced lung injury model.Pediatric research · 2025Article
- An overview of CCN4 (WISP1) role in human diseases.Journal of translational medicine · 2024Review
- Notch signaling regulates pulmonary fibrosis.Frontiers in cell and developmental biology · 2024Review
- A systematic review of the research progress of traditional Chinese medicine against pulmonary fibrosis: from a pharmacological perspective.Chinese medicine · 2023Review
- Ginseng saponin metabolite 20(S)-protopanaxadiol relieves pulmonary fibrosis by multiple-targets signaling pathways.Journal of ginseng research · 2023Article
- Cross-Talk between Wnt Signaling and Src Tyrosine Kinase.Biomedicines · 2022Review
- TRAF6 Suppresses the Development of Pulmonary Fibrosis by Attenuating the Activation of Fibroblasts.Frontiers in pharmacology · 2022Article
- Nintedanib and Dasatinib Treatments Induce Protective Autophagy as a Potential Resistance Mechanism in MPM Cells.Frontiers in cell and developmental biology · 2022Article
- Silibinin Suppresses Tumor Cell-Intrinsic Resistance to Nintedanib and Enhances Its Clinical Activity in Lung Cancer.Cancers · 2021Article
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Idiopathic pulmonary fibrosis (IPF) is an interstitial lung disease characterized by epithelial cell damage, myofibroblast activation, and collagen deposition. Multiple studies have documented that the Wnt/β-catenin pathway is aberrantly activated in IPF and plays a vital role in myofibroblast differentiation and activation. Kinases such as Src initiate Wnt/β-catenin signaling by phosphorylating β-catenin at tyrosine residues, which facilitates β-catenin accumulation in the nucleus and promotion of fibrosis progression. Nintedanib has been approved for the treatment of IPF as a multitargeted tyrosine kinase inhibitor. Nintedanib has been demonstrated to directly block Src, and whether it attenuates pulmonary fibrosis through regulating the Wnt/β-catenin pathway remains unclear. In this study, we found that nintedanib attenuated myofibroblast activation through inhibiting the expression of genes downstream of Wnt signaling such as Cyclin D1, Wisp1, and S100a4. Further experiments showed that nintedanib inhibited Wnt3a-induced β-catenin nuclear translocation through suppressing Src kinase activation and β-catenin Y654 phosphorylation. Additionally, Src knockdown fibroblasts exhibited a phenotype similar to that of the nintedanib treatment group, and the inhibitory effects of nintedanib were consistent with those of the Src kinase inhibitor KX2-391. In summary, our study shows that nintedanib exhibits an anti-fibrosis effect, partly by inhibiting the Src/β-catenin pathway.
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