ArticlePloS one2011
Complement and the alternative pathway play an important role in LPS/D-GalN-induced fulminant hepatic failure.
Article in PloS one, 2011. 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, 43 citations in OpenAlex.
- Research progress on the roles of complement in liver injury.World journal of hepatology · 2025Review
- Thrombospondin 1 enhances systemic inflammation and disease severity in acute-on-chronic liver failure.BMC medicine · 2024Article
- Contribution of animal models to the mechanistic understanding of Alternative Pathway and Amplification Loop (AP/AL)-driven Complement-mediated Diseases.Immunological reviews · 2023Review
- New Insights into the Role of the Complement System in Human Viral Diseases.Biomolecules · 2022Review
- Dihydro-stilbene gigantol relieves CClActa pharmacologica Sinica · 2020Article
- The Role of Complement in Liver Injury, Regeneration, and Transplantation.Hepatology (Baltimore, Md.) · 2019Review
- Tissue-targeted complement therapeutics.Molecular immunology · 2018Review
- Article
- Complement System as a Target for Therapies to Control Liver Regeneration/Damage in Acute Liver Failure Induced by Viral Hepatitis.Journal of immunology research · 2018Article
- The hepatic "matrisome" responds dynamically to injury: Characterization of transitional changes to the extracellular matrix in mice.Hepatology (Baltimore, Md.) · 2017Article
- C5a/C5aR pathway is essential for up-regulating SphK1 expression through p38-MAPK activation in acute liver failure.World journal of gastroenterology · 2016Article
- [Association between protective effect of Liuwei Wuling tablets against acute liver injury and its inhibitory effect on cytoplasmic translocation of high-mobility group box-1 in hepatocytes in mice].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2016Article
- Complement Factor 3 Could Be an Independent Risk Factor for Mortality in Patients with HBV Related Acute-on-Chronic Liver Failure.BioMed research international · 2016Observational
- Article
- Circulating mannan-binding lectin, M-, L-, H-ficolin and collectin-liver-1 levels in patients with acute liver failure.Liver international : official journal of the International Association for the Study of the Liver · 2015Article
- Employment of digital gene expression profiling to identify potential pathogenic and therapeutic targets of fulminant hepatic failure.Journal of translational medicine · 2015Article
- Complement receptors C5aR and C5L2 are associated with metabolic profile, sex hormones, and liver enzymes in obese women pre- and postbariatric surgery.Journal of obesity · 2014Article
Corrections and comments
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Authors and funding
16 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fulminant hepatic failure (FHF) is a clinically severe type of liver injury with an extremely high mortality rate. Although the pathological mechanisms of FHF are not well understood, evidence suggests that the complement system is involved in the pathogenesis of a variety of liver disorders. In the present study, to investigate the role of complement in FHF, we examined groups of mice following intraperitoneal injection of LPS/D-GalN: wild-type C57BL/6 mice, wild-type mice treated with a C3aR antagonist, C5aR monoclonal antibody (C5aRmAb) or CR2-Factor H (CR2-fH, an inhibitor of the alternative pathway), and C3 deficient mice (C3⁻/⁻ mice). The animals were euthanized and samples analyzed at specific times after LPS/D-GalN injection. The results show that intraperitoneal administration of LPS/D-GalN activated the complement pathway, as evidenced by the hepatic deposition of C3 and C5b-9 and elevated serum levels of the complement activation product C3a, the level of which was associated with the severity of the liver damage. C3a receptor (C3aR) and C5a receptor (C5aR) expression was also upregulated. Compared with wild-type mice, C3⁻/⁻ mice survived significantly longer and displayed reduced liver inflammation and attenuated pathological damage following LPS/D-GalN injection. Similar levels of protection were seen in mice treated with C3aR antagonist,C5aRmAb or CR2-fH. These data indicate an important role for the C3a and C5a generated by the alternative pathway in LPS/D-GalN-induced FHF. The data further suggest that complement inhibition may be an effective strategy for the adjunctive treatment of fulminant hepatic failure.
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