ArticleImmunology2013
Complement 5a stimulates hepatic stellate cells in vitro, and is increased in the plasma of patients with chronic hepatitis B.
Article in Immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 27 citations in OpenAlex.
- Damaged glomeruli in proliferative pediatric lupus nephritis exhibit a C5a-C5aR1 induced fibrotic transcriptional program.bioRxiv : the preprint server for biology · 2026Article
- Research progress on the roles of complement in liver injury.World journal of hepatology · 2025Review
- Blockade of C5aR1 alleviates liver inflammation and fibrosis in a mouse model of NASH by regulating TLR4 signaling and macrophage polarization.Journal of gastroenterology · 2023Article
- GPCRs and fibroblast heterogeneity in fibroblast-associated diseases.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Review
- Immune response and treatment targets of chronic hepatitis B virus infection: innate and adaptive immunity.Frontiers in cellular and infection microbiology · 2023Review
- A pilot study on some critical immune elements in HBV infection: evidence of Alpha-1 Antitrypsin as an immunological biomarker.Gastroenterology and hepatology from bed to bench · 2022Article
- Complement factors C3a and C5a mimick a proinflammatory microenvironment and increase HBV IGRA sensitivity.Journal of translational medicine · 2019Article
- HBV-Induced Immune Imbalance in the Development of HCC.Frontiers in immunology · 2019Review
- IP-10 Expression in Patients with Chronic HBV Infection and Its Ability to Predict the Decrease in HBsAg Levels after Treatment with Entecavir.Molecules and cells · 2017Article
- Complement 5a is an indicator of significant fibrosis and earlier cirrhosis in patients chronically infected with hepatitis B virus.Infection · 2017Article
- Complement Component 5 Mediates Development of Fibrosis, via Activation of Stellate Cells, in 2 Mouse Models of Chronic Pancreatitis.Gastroenterology · 2015Article
- Cellular and molecular functions of hepatic stellate cells in inflammatory responses and liver immunology.Hepatobiliary surgery and nutrition · 2014Review
- Complement factor C5 but not C3 contributes significantly to hydrosalpinx development in mice infected with Chlamydia muridarum.Infection and immunity · 2014Article
- Anaphylatoxin C5a modulates hepatic stellate cell migration.Fibrogenesis & tissue repair · 2014Article
- Mannan-binding lectin suppresses growth of hepatocellular carcinoma by regulating hepatic stellate cell activationOncoimmunologyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Complement 5a (C5a) is a critical modulator of liver immunity. In this study, we investigated the role of C5a and its receptor in liver fibrosis in patients with hepatitis B virus infection. We found that plasma C5a concentration was significantly increased in patients with chronic hepatitis B, particularly in those patients with higher grade and stage scores. Further analysis indicated that the increased C5a concentration was positively correlated with clinical parameters reflecting liver fibrosis severity, including type IV collagen and procollagen type III N-terminal peptide. Our in vitro data indicated that the C5a receptor is highly expressed in hepatic stellate cells (HSCs). Addition of C5a significantly activated HSCs and up-regulated α-smooth muscle actin, hyaluronic acid and type IV collagen expression. Also, addition of C5a could inhibit the spontaneous and soluble tumour necrosis factor-related apoptosis-inducing ligand-induced apoptosis of HSCs. These findings highlight the potential role of C5a in the regulation of liver fibrosis.
Indexed as
Identifiers
What OpenQuestion holds
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.