The DOI matches its Crossref record; 11 of the 11 references it cites were found in a registry or an index.
The role of tyrosine kinases in the pathogenesis of idiopathic pulmonary fibrosis
Abstract
Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease with a median survival time from diagnosis of 2–3 years. Although the pathogenic pathways have not been fully elucidated, IPF is believed to be caused by persistent epithelial injury in genetically susceptible individuals. Tyrosine kinases are involved in a range of signalling pathways that are essential for cellular homeostasis. However, there is substantial evidence from in vitro studies and animal models that receptor tyrosine kinases, such as the platelet-derived growth factor receptor, vascular endothelial growth factor receptor and fibroblast growth factor receptor, and non-receptor tyrosine kinases, such as the Src family, play critical roles in the pathogenesis of pulmonary fibrosis. For example, the expression and release of tyrosine kinases are altered in patients with IPF, while specific tyrosine kinases stimulate the proliferation of lung fibroblasts in vitro. Agents that inhibit tyrosine kinases have shown anti-fibrotic and anti-inflammatory effects in animal models of pulmonary fibrosis. Recently, the tyrosine kinase inhibitor nintedanib has shown positive results in two phase III trials in patients with IPF. Here, we summarise the evidence for involvement of specific tyrosine kinases in the pathogenesis of IPF and the development of tyrosine kinase inhibitors as treatments for IPF.
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Cites
Efficacy and Safety of Nintedanib in Idiopathic Pulmonary Fibrosis
Richeldi, L., du Bois, R. M., Raghu, G., Azuma, A., Brown, K. K., Costabel, U., Cottin, V., Flaherty, K. R., Hansell, D. M., Inoue, Y., et al. (2014) · New England Journal of Medicine · doi:10.1056/nejmoa1402584 · Cited by 4,654
A phase 3 trial of pirfenidone in patients with idiopathic pulmonary fibrosis.
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VEGF receptor signalling ? in control of vascular function
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Efficacy of a Tyrosine Kinase Inhibitor in Idiopathic Pulmonary Fibrosis
Richeldi, L., Costabel, U., Selman, M., Kim, D. S., Hansell, D. M., Nicholson, A. G., Brown, K. K., Flaherty, K. R., Noble, P. W., Raghu, G., et al. (2011) · New England Journal of Medicine · doi:10.1056/nejmoa1103690 · Cited by 1,157
BIBF 1120: Triple Angiokinase Inhibitor with Sustained Receptor Blockade and Good Antitumor Efficacy
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Imatinib Treatment for Idiopathic Pulmonary Fibrosis: Randomized Placebo-controlled Trial Results
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Cited by
Idiopathic pulmonary fibrosis: pathogenesis and management
Sgalla, G., Iovene, B., Calvello, M., Ori, M., Varone, F., & Richeldi, L. (2018) · Respiratory Research · doi:10.1186/s12931-018-0730-2 · Cited by 573
Idiopathic Pulmonary Fibrosis: An Update on Pathogenesis
Mei, Q., Liu, Z., Zuo, H., Yang, Z., & Qu, J. (2022) · Frontiers in Pharmacology · doi:10.3389/fphar.2021.797292 · Cited by 360
The Bleomycin Model of Pulmonary Fibrosis
Liu, T., De Los Santos, F. G., & Phan, S. H. (2017) · Methods in Molecular Biology · doi:10.1007/978-1-4939-7113-8_2 · Cited by 357
Idiopathic Pulmonary Fibrosis and Lung Cancer: Mechanisms and Molecular Targets
Ballester, B., Milara, J., & Cortijo, J. (2019) · International Journal of Molecular Sciences · doi:10.3390/ijms20030593 · Cited by 308
TGF‐β as a driver of fibrosis: physiological roles and therapeutic opportunities
Budi, E. H., Schaub, J. R., Decaris, M., Turner, S., & Derynck, R. (2021) · The Journal of Pathology · doi:10.1002/path.5680 · Cited by 292
Metadata
- Authors
- Grimminger, F., Günther, A., & Vancheri, C.
- Venue
- European Respiratory Journal
- Publisher
- European Respiratory Society (ERS)
- Published
- 2015-03-05
- Volume
- 45
- Issue
- 5
- Pages
- 1426-1433
- ISSN
- 0903-1936 (ISSN-L)
- 1399-3003
- OpenAlex
- W2001818756
- Cited by
- 178
- References
- 11
- FWCI
- 9.99
- Type
- journal article
- Language
- en
- Open access
- closed
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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