ArticleInflammatory bowel diseases2021
AXL Is a Potential Target for the Treatment of Intestinal Fibrosis.
Article in Inflammatory bowel diseases, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 47 citations in OpenAlex.
- Discoidin domain receptor 1 (DDR1): An emerged novel mechanosensor.Fundamental research · 2026Review
- Review on advances in small molecule inhibitors on the treatment of inflammatory bowel disease.Molecular biology reports · 2026Review
- Discovery of novel biomarkers associated with myocardial fibrosis in chimpanzees (Frontiers in veterinary science · 2026Article
- PDGFRαAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Evaluation of TAM Receptor Targeting in Pathophysiology of Idiopathic Pulmonary Fibrosis.Medicina (Kaunas, Lithuania) · 2025Article
- Targeted Therapies Modulating Mesenchymal-Epithelial Transition-Linked Oncogenic Signaling in the Tumor Microenvironment: Comparative Profiling of Capmatinib, Bemcentinib, and Galunisertib.Journal of clinical medicine · 2025Review
- Growth arrest specific-6 and angiotoxin receptor-like signaling drive oral regenerative wound repair.Science translational medicine · 2025Article
- Clearing the Path: Exploring Apoptotic Cell Clearance in Inflammatory and Autoimmune Disorders for Therapeutic Advancements.Molecular biotechnology · 2025Review
- Phytochemical Compounds as Promising Therapeutics for Intestinal Fibrosis in Inflammatory Bowel Disease: A Critical Review.Nutrients · 2024Review
- Osteopontin regulation of MerTKiScience · 2024Article
- Preventing fibrosis in IBD: update on immune pathways and clinical strategies.Expert review of clinical immunology · 2024Review
- Inflammation accelerating intestinal fibrosis: from mechanism to clinic.European journal of medical research · 2024Review
- mFrontiers of medicine · 2024Article
- Mechanisms and therapeutic research progress in intestinal fibrosis.Frontiers in medicine · 2024Article
- Anti-fibrotics in inflammatory bowel diseases: Challenges and successes.Advances in pharmacology (San Diego, Calif.) · 2024Review
- Prospective therapeutics for intestinal and hepatic fibrosis.Bioengineering & translational medicine · 2023Review
- The TNFThe American journal of pathology · 2023Article
- Gas6/TAM Axis Involvement in Modulating Inflammation and Fibrosis in COVID-19 Patients.International journal of molecular sciences · 2023Review
- Levocarnitine regulates the growth of angiotensin II-induced myocardial fibrosis cells via TIMP-1.Open life sciences · 2023Article
- Hypoxia-inducible factor as a bridge between healthy barrier function, wound healing, and fibrosis.American journal of physiology. Cell physiology · 2022Review
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
backgroundFibrosis is the final common pathway to intestinal failure in Crohn's disease, but no medical therapies exist to treat intestinal fibrosis. Activated myofibroblasts are key effector cells of fibrosis in multiple organ systems, including the intestine. AXL is a receptor tyrosine kinase that has been implicated in fibrogenic pathways involving myofibroblast activation. We aimed to investigate the AXL pathway as a potential target for the treatment of intestinal fibrosis.
methodsTo establish proof of concept, we first analyzed AXL gene expression in 2 in vivo models of intestinal fibrosis and 3 in vitro models of intestinal fibrosis. We then tested whether pharmacological inhibition of AXL signaling could reduce fibrogenesis in 3 in vitro models of intestinal fibrosis. In vitro testing included 2 distinct cell culture models of intestinal fibrosis (matrix stiffness and TGF-β1 treatment) and a human intestinal organoid model using TGF-β1 cytokine stimulation.
resultsOur findings suggest that the AXL pathway is induced in models of intestinal fibrosis. We demonstrate that inhibition of AXL signaling with the small molecule inhibitor BGB324 abrogates both matrix-stiffness and transforming growth factor beta (TGF-β1)-induced fibrogenesis in human colonic myofibroblasts. AXL inhibition with BGB324 sensitizes myofibroblasts to apoptosis. Finally, AXL inhibition with BGB324 blocks TGF-β1-induced fibrogenic gene and protein expression in human intestinal organoids.
conclusionsThe AXL pathway is active in multiple models of intestinal fibrosis. In vitro experiments suggest that inhibiting AXL signaling could represent a novel approach to antifibrotic therapy for intestinal fibrosis such as in Crohn's disease.
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