ArticleDisease models & mechanisms2022
Therapeutic potential of macrophage colony-stimulating factor in chronic liver disease.
Article in Disease models & mechanisms, 2022. 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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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
13 citing papers in PubMed, 17 citations in OpenAlex.
- Regulatory roles and translational potential of the Kruppel-like factor family in liver disease.iLIVER · 2026Review
- Coffee Consumption and Improved Liver Outcomes: Clinical, Imaging, and Proteomic Evidence From the UK Biobank.Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association · 2026Article
- Administration of human macrophage colony-stimulating factor-mFc fusion protein increases macrophage phagocytic capacity and stimulates liver regeneration in mice.Journal of inflammation (London, England) · 2026Article
- Integrated WGCNA of lncRNA-mRNA Networks Identifies Novel Hub Genes and Potential Therapeutic Agents for Liver Cirrhosis via Molecular Docking Validation.International journal of molecular sciences · 2026Article
- Diagnostic and Prognostic Biomarkers for Sepsis-Associated Liver Injury: Current Status and Future Perspectives.Gastroenterology research and practice · 2026Review
- Article
- Chromatin dynamics and regulatory drivers of hypoplastic hepatic progenitor cells in partial hepatectomy model.Communications biology · 2025Article
- Perisurgical colony stimulating factor one treatment ameliorates liver ischaemia/reperfusion injury in rats.World journal of gastroenterology · 2025Article
- Wild-type bone marrow cells repopulate tissue resident macrophages and reverse the impacts of homozygous CSF1R mutation.PLoS genetics · 2025Article
- The multifaceted role of macrophages during acute liver injury.Frontiers in immunology · 2023Review
- CSF1R as a Therapeutic Target in Bone Diseases: Obvious but Not so Simple.Current osteoporosis reports · 2022Review
- A kinase-dead Csf1r mutation associated with adult-onset leukoencephalopathy has a dominant inhibitory impact on CSF1R signalling.Development (Cambridge, England) · 2022Article
- Correlation of Serum M-CSF, CER, and TIMP-1 Levels with Liver Fibrosis in Viral Hepatitis.Computational and mathematical methods in medicine · 2022Article
Corrections and comments
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Authors and funding
18 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Resident and recruited macrophages control the development and proliferation of the liver. We have previously shown in multiple species that treatment with a macrophage colony stimulating factor (CSF1)-Fc fusion protein initiated hepatocyte proliferation and promoted repair in models of acute hepatic injury in mice. Here, we investigated the impact of CSF1-Fc on resolution of advanced fibrosis and liver regeneration, using a non-resolving toxin-induced model of chronic liver injury and fibrosis in C57BL/6J mice. Co-administration of CSF1-Fc with exposure to thioacetamide (TAA) exacerbated inflammation consistent with monocyte contributions to initiation of pathology. After removal of TAA, either acute or chronic CSF1-Fc treatment promoted liver growth, prevented progression and promoted resolution of fibrosis. Acute CSF1-Fc treatment was also anti-fibrotic and pro-regenerative in a model of partial hepatectomy in mice with established fibrosis. The beneficial impacts of CSF1-Fc treatment were associated with monocyte-macrophage recruitment and increased expression of remodelling enzymes and growth factors. These studies indicate that CSF1-dependent macrophages contribute to both initiation and resolution of fibrotic injury and that CSF1-Fc has therapeutic potential in human liver disease.
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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.