ArticleAmerican journal of respiratory cell and molecular biology2021
Targeting the AXL Receptor in Combating Smoking-related Pulmonary Fibrosis.
Article in American journal of respiratory cell and molecular biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- Targeting receptor tyrosine kinases: from molecular mechanisms to clinical therapeutics.Signal transduction and targeted therapy · 2026Review
- Discovery of novel biomarkers associated with myocardial fibrosis in chimpanzees (Frontiers in veterinary science · 2026Article
- Evaluation of TAM Receptor Targeting in Pathophysiology of Idiopathic Pulmonary Fibrosis.Medicina (Kaunas, Lithuania) · 2025Article
- Inhibition of AXL ameliorates pulmonary fibrosisThe European respiratory journal · 2025Article
- Targeting the AXL pathway: a promising strategy for pulmonary fibrosis.The European respiratory journal · 2025Article
- Recent advances in TAM mechanisms in lung diseases.Journal of translational medicine · 2025Review
- Orderly Regulation of Macrophages and Fibroblasts by Axl in Bleomycin-Induced Pulmonary Fibrosis in Mice.Journal of cellular and molecular medicine · 2025Article
- Elevated Plasma Levels of Growth Arrest Specific 6 (Gas6) Protein in Severe Obesity: Implications for Adipose Tissue and Inflammation.Medical science monitor : international medical journal of experimental and clinical research · 2024Article
- mFrontiers of medicine · 2024Article
- Targeting CD301EMBO molecular medicine · 2023Article
- A Review: The Potential Involvement of Growth Arrest-Specific 6 and Its Receptors in the Pathogenesis of Lung Damage and in Coronavirus Disease 2019.Microorganisms · 2023Review
- Inositol possesses antifibrotic activity and mitigates pulmonary fibrosis.Respiratory research · 2023Article
- Gas6/TAM Axis Involvement in Modulating Inflammation and Fibrosis in COVID-19 Patients.International journal of molecular sciences · 2023Review
- Article
- Soluble ECM promotes organotypic formation in lung alveolar model.Biomaterials · 2022Article
- Virtual screening and activity evaluation of multitargeting inhibitors for idiopathic pulmonary fibrosis.Frontiers in pharmacology · 2022Article
- The Role of Hepatic Stellate Cells and the Gas6/Axl Axis in Liver Fibrosis and Hepatocellular Carcinoma.Journal of clinical and experimental hepatologyArticle
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Tobacco smoking is a well-known risk factor for both fibrogenesis and fibrotic progression; however, the mechanisms behind these processes remain enigmatic. RTKs (receptor tyrosine kinases) have recently been reported to drive profibrotic phenotypes in fibroblasts during pulmonary fibrosis (PF). Using a phospho-RTK array screen, we identified the RTK AXL as a top upregulated RTK in response to smoke. Both expression and signaling activity of AXL were indeed elevated in lung fibroblasts exposed to tobacco smoke, whereas no significant change to the levels of a canonical AXL ligand, Gas6 (growth arrest-specific 6), was seen upon smoke treatment. Notably, we found that smoke-exposed human lung fibroblasts exhibited highly proliferative and invasive activities and were capable of inducing fibrotic lung lesions in mice. Conversely, genetic suppression of AXL in smoke-exposed fibroblasts cells led to suppression of AXL downstream pathways and aggressive phenotypes. We further demonstrated that AXL interacted with MARCKS (myristoylated alanine-rich C kinase substrate) and cooperated with MARCKS in regulating downstream signaling activity and fibroblast invasiveness. Pharmacological inhibition of AXL with AXL-specific inhibitor R428 showed selectivity for smoke-exposed fibroblasts. In all, our data suggest that AXL is a potential marker for smoke-associated PF and that targeting of the AXL pathway is a potential therapeutic strategy in treating tobacco smoking-related PF.
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Registered trials
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.