ArticleThe Journal of clinical investigation2020
Complement factor H-deficient mice develop spontaneous hepatic tumors.
Article in The Journal of clinical investigation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 62 citations in OpenAlex.
- miR-22-Galectin-1 as an integral signaling axis in regulating metabolism and immunity in HCC.Biomarker research · 2026Article
- Article
- Friend or foe: assessing the value of animal models for facilitating clinical breakthroughs in complement research.The Journal of clinical investigation · 2025Review
- Chronic kidney disease enhances alternative pathway activity: a new paradigm.The Journal of clinical investigation · 2025Review
- Diagnosis and Staging of Metabolic Dysfunction-Associated Steatotic Liver Disease Using Biomarker-Directed Aptamer Panels.Biomolecules · 2025Article
- Complement or insult: the emerging link between complement cascade deficiencies and pathology of myeloid malignancies.Journal of leukocyte biology · 2024Review
- Role of Complement in Liver Diseases.Seminars in liver disease · 2024Review
- Complement factor H in molecular regulation of angiogenesis.Medical review (2021) · 2024Review
- Complement C3a/C3aR inhibition alleviates the formation of aortic aneurysm in Marfan syndrome mice.BMC cardiovascular disorders · 2024Article
- Factor H's Control of Complement Activation Emerges as a Significant and Promising Therapeutic Target for Alzheimer's Disease Treatment.International journal of molecular sciences · 2024Article
- Complement factor H: a novel innate immune checkpoint in cancer immunotherapy.Frontiers in cell and developmental biology · 2024Review
- The human factor H protein family - an update.Frontiers in immunology · 2024Review
- Interplay of Extracellular Vesicles and TLR4 Signaling in Hepatocellular Carcinoma Pathophysiology and Therapeutics.Pharmaceutics · 2023Review
- Roles of Extracellular Vesicles on the Progression and Metastasis of Hepatocellular Carcinoma.Cells · 2023Review
- Clinical characterization and proteomic profiling of lean nonalcoholic fatty liver disease.Frontiers in endocrinology · 2023Article
- Alternative pathway diagnostics.Immunological reviews · 2023Review
- Prediction of liver cancer prognosis based on immune cell marker genes.Frontiers in immunology · 2023Article
- Proteomic analysis of small extracellular vesicles from the plasma of patients with hepatocellular carcinoma.World journal of surgical oncology · 2022Article
- Factor H related proteins modulate complement activation on kidney cells.Kidney international · 2022Article
- Macrophages as tools and targets in cancer therapy.Nature reviews. Drug discovery · 2022Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 3 countries.
Funding
Abstract
Hepatocellular carcinoma (HCC) is difficult to detect, carries a poor prognosis, and is one of few cancers with an increasing yearly incidence. Molecular defects in complement factor H (CFH), a critical regulatory protein of the complement alternative pathway (AP), are typically associated with inflammatory diseases of the eye and kidney. Little is known regarding the role of CFH in controlling complement activation within the liver. While studying aging CFH-deficient (fH-/-) mice, we observed spontaneous hepatic tumor formation in more than 50% of aged fH-/- males. Examination of fH-/- livers (3-24 months) for evidence of complement-mediated inflammation revealed widespread deposition of complement-activation fragments throughout the sinusoids, elevated transaminase levels, increased hepatic CD8+ and F4/80+ cells, overexpression of hepatic mRNA associated with inflammatory signaling pathways, steatosis, and increased collagen deposition. Immunostaining of human HCC biopsies revealed extensive deposition of complement fragments within the tumors. Investigating the Cancer Genome Atlas also revealed that increased CFH mRNA expression is associated with improved survival in patients with HCC, whereas mutations are associated with worse survival. These results indicate that CFH is critical for controlling complement activation in the liver, and in its absence, AP activation leads to chronic inflammation and promotes hepatic carcinogenesis.
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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.