ArticleHepatology (Baltimore, Md.)2017
Hepatitis C virus-induced CCL5 secretion from macrophages activates hepatic stellate cells.
Article in Hepatology (Baltimore, Md.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.
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
48 citing papers in PubMed, 1 synthesis or guideline pooled it, 75 citations in OpenAlex.
- Inflammasomes and their roles in the pathogenesis of viral hepatitis and their related complications: An updated systematic review.Immunology letters · 2019Pooled it
- Identification of Promising Candidate Genes and Immune Infiltration Patterns in Chronic Schistosomiasis-Associated Liver Injury by WGCNA and Machine Learning.Pathogens (Basel, Switzerland) · 2026Article
- ZDHHC17-mediated IKKβ palmitoylation suppresses NF-κB signaling to mitigate the progression of liver fibrosis.iScience · 2026Article
- Liver Macrophages in the Pathogenesis of Viral Hepatitis.Current issues in molecular biology · 2026Review
- The Gut-Immune Axis in Treated HIV Infection: From Mucosal Damage to Chronic Inflammation and Therapeutic Opportunities-A Clinician-Oriented Narrative Review.Microorganisms · 2026Review
- Nuclear Factor I-B Delays Liver Fibrosis by Inhibiting Chemokine Ligand 5 Transcription.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Nanoparticle-based systems for liver therapy: Overcoming fibrosis and enhancing drug efficacy.World journal of hepatology · 2025Review
- The role of liver macrophages in viral liver pathogenesis.Journal of leukocyte biology · 2025Review
- NLRP3 inflammasome inhibition decreasesInfection and immunity · 2024Article
- Viral Hepatitis: Host Immune Interaction, Pathogenesis and New Therapeutic Strategies.Pathogens (Basel, Switzerland) · 2024Review
- Integrated multi-omics profiling landscape of organising pneumonia.Clinical and translational medicine · 2024Article
- Metabolic Dysfunction-Associated Fatty Liver Disease and Chronic Viral Hepatitis: The Interlink.Pathogens (Basel, Switzerland) · 2024Review
- Common molecular basis for MASH and hepatitis C revealed via systems biology approach.Frontiers in oncology · 2024Article
- Hepatitis C Virus and the Host: A Mutual Endurance Leaving Indelible Scars in the Host's Immunity.International journal of molecular sciences · 2023Review
- Insights on drug and gene delivery systems in liver fibrosis.Asian journal of pharmaceutical sciences · 2023Review
- Thymosin Beta 4 Inhibits LPS and ATP-Induced Hepatic Stellate Cells via the Regulation of Multiple Signaling Pathways.International journal of molecular sciences · 2023Article
- The Ultrastructure of Hepatic Stellate Cell-Macrophage Intercellular Crosstalk as a New Morphological Insight into Phenomenon of Fibrogenesis in Pediatric Autoimmune Hepatitis.Journal of clinical medicine · 2023Article
- Molecular Changes in Relation to Alcohol Consumption and Hepatocellular Carcinoma.International journal of molecular sciences · 2022Review
- Circulatory Exosomes from COVID-19 Patients Trigger NLRP3 Inflammasome in Endothelial Cells.mBio · 2022Article
- Hepatitis C Virus Alters Macrophage Cholesterol Metabolism Through Interaction with Scavenger Receptors.Viral immunology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Hepatitis C virus (HCV)-mediated chronic liver disease is a serious health problem around the world and often causes fibrosis/cirrhosis and hepatocellular carcinoma. The mechanism of liver disease progression during HCV infection is still unclear, although inflammation is believed to be an important player in disease pathogenesis. We previously reported that macrophages including Kupffer cells exposed to HCV induce proinflammatory cytokines. These secreted cytokines may activate hepatic stellate cells (HSCs) toward fibrosis. In this study, we examined crosstalk between macrophages and HSCs following HCV infection. Primary human HSCs and immortalized HSCs (LX2 cells) were incubated with conditioned medium derived from HCV-exposed human macrophages. Expression of inflammasome and fibrosis-related genes in these cells was examined, with increased expression of inflammatory (NLR family pyrin domain containing 3, interleukins 1β and 6, and cysteine-cysteine chemokine ligand 5 [CCL5]) and profibrogenic (transforming growth factor β1, collagen type 4 alpha 1, matrix metalloproteinase 2, and alpha-smooth muscle actin) markers. Further investigation suggested that CCL5, secreted from HCV-exposed macrophages, activates inflammasome and fibrosis markers in HSCs and that neutralizing antibody to CCL5 inhibited activation.
conclusionTogether, our results demonstrate that human macrophages exposed to HCV induce CCL5 secretion, which plays a significant role in hepatic inflammation and fibrosis. (Hepatology 2017;66:746-757).
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.