ArticleJCI insight2023
CCL24 regulates biliary inflammation and fibrosis in primary sclerosing cholangitis.
Article in JCI insight, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
20 citing papers in PubMed, 36 citations in OpenAlex.
- Hepatocyte TrkB Acts as a Gatekeeper Against MASH-Related Liver Fibrosis by Suppressing the TGFβ/CCL2 Axis and Macrophage Infiltration.Cell proliferation · 2026Article
- Gut microbiota in health and disease.Molecular biomedicine · 2026Review
- Cholangiocyte biology in primary sclerosing cholangitis and other cholangiopathies: pathogenesis, clinical insights, and experimental tools.Physiological reviews · 2026Review
- Non-reproductive tumor progression impairs ovarian function through CXCL10-IL18R1 axis.Experimental & molecular medicine · 2026Article
- Unravelling mesenteric fibrosis in small intestinal neuroendocrine tumours and implications for clinical management.Endocrine-related cancer · 2026Review
- Prognostic implications and molecular mechanisms of derived organoid-angiogenesis-related genes (DOARGs) in colorectal cancer.Journal of physiology and biochemistry · 2026Article
- Next-Generation Hydrogels for Biliary Organoid Engineering.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Macrophage-Derived CCL24 Promotes Cardiac Fibrosis Via Fibroblast CCR3.Circulation research · 2025Article
- Mechanisms and targeted prevention of abnormal ductular reaction caused by a low concentration of Benzo(a)pyrene.Cell death & disease · 2025Article
- Bioengineered Tumor-Derived Extracellular Vehicles Suppressed Colorectal Cancer Liver Metastasis and Bevacizumab Resistance.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Portal Fibrosis and the Ductular Reaction: Pathophysiological Role in the Progression of Liver Disease and Translational Opportunities.Gastroenterology · 2025Review
- Soluble Factors and Mechanisms Regulated by Sialylated IgG Signaling.Immunological reviews · 2025Review
- Review
- Macrophage heterogeneity in liver fibrosis.Frontiers in immunology · 2025Review
- Current status of pharmacotherapy for primary sclerosing cholangitis.Frontiers in medicine · 2025Review
- Mechanism-guided drug development and treatment for liver fibrosis: a clinical perspective.Frontiers in pharmacology · 2025Review
- Molecular Mechanisms of Fibrosis in Cholestatic Liver Diseases and Regenerative Medicine-Based Therapies.Cells · 2024Review
- Article
- Machine Learning Identifies Key Proteins in Primary Sclerosing Cholangitis Progression and Links High CCL24 to Cirrhosis.International journal of molecular sciences · 2024Article
- The Role of CCL24 in Primary Sclerosing Cholangitis: Bridging Patient Serum Proteomics to Preclinical Data.Cells · 2024Article
Corrections and comments
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Authors and funding
24 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
ˆCCL24 is a pro-fibrotic, pro-inflammatory chemokine expressed in several chronic fibrotic diseases. In the liver, CCL24 plays a role in fibrosis and inflammation, and blocking CCL24 led to reduced liver injury in experimental models. We studied the role of CCL24 in primary sclerosing cholangitis (PSC) and evaluated the potential therapeutic effect of blocking CCL24 in this disease. Multidrug resistance gene 2-knockout (Mdr2-/-) mice demonstrated CCL24 expression in liver macrophages and were used as a relevant experimental PSC model. CCL24-neutralizing monoclonal antibody, CM-101, significantly improved inflammation, fibrosis, and cholestasis-related markers in the biliary area. Moreover, using spatial transcriptomics, we observed reduced proliferation and senescence of cholangiocytes following CCL24 neutralization. Next, we demonstrated that CCL24 expression was elevated under pro-fibrotic conditions in primary human cholangiocytes and macrophages, and it induced proliferation of primary human hepatic stellate cells and cholangiocytes, which was attenuated following CCL24 inhibition. Correspondingly, CCL24 was found to be highly expressed in liver biopsies of patients with PSC. CCL24 serum levels correlated with Enhanced Liver Fibrosis score, most notably in patients with high alkaline phosphatase levels. These results suggest that blocking CCL24 may have a therapeutic effect in patients with PSC by reducing liver inflammation, fibrosis, and cholestasis.
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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.