ArticleScientific reports2013
HCV NS3 protease enhances liver fibrosis via binding to and activating TGF-β type I receptor.
Article in Scientific reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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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
21 citing papers in PubMed, 37 citations in OpenAlex.
- Liver Macrophages in the Pathogenesis of Viral Hepatitis.Current issues in molecular biology · 2026Review
- The role of liver macrophages in viral liver pathogenesis.Journal of leukocyte biology · 2025Review
- Hepatitis C Virus-Core Antigen: Implications in Diagnostic, Treatment Monitoring and Clinical Outcomes.Viruses · 2024Review
- From viruses to cancer: exploring the role of the hepatitis C virus NS3 protein in carcinogenesis.Infectious agents and cancer · 2024Review
- Hepatitis B and Hepatitis C Virus Infection Promote Liver Fibrogenesis through a TGF-β1-Induced OCT4/Nanog Pathway.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Micro-PET imaging of hepatitis C virus NS3/4A protease activity using a protease-activatable retention probe.Frontiers in microbiology · 2022Article
- Regression of Hepatic Fibrosis and Evolution of Cirrhosis: A Concise Review.Advances in anatomic pathology · 2021Review
- Review
- Molecular Crosstalk between the Hepatitis C Virus and the Extracellular Matrix in Liver Fibrogenesis and Early Carcinogenesis.Cancers · 2021Review
- Induced hepatic stellate cell integrin, α8β1, enhances cellular contractility and TGFβ activity in liver fibrosis.The Journal of pathology · 2021Article
- LPS stimulation during HCV infection induces MMP/TIMP1 imbalance in macrophages.Journal of medical microbiology · 2020Article
- Hepatitis C Virus and Hepatocellular Carcinoma: When the Host Loses Its Grip.International journal of molecular sciences · 2020Review
- Transforming Growth Factor β Acts as a Regulatory Molecule for Lipogenic Pathways among Hepatitis C Virus Genotype-Specific Infections.Journal of virology · 2019Article
- Development of latent Interferon alpha 2b as a safe therapeutic for treatment of Hepatitis C virus infection.Scientific reports · 2019Article
- Identification of Piperazinylbenzenesulfonamides as New Inhibitors of Claudin-1 Trafficking and Hepatitis C Virus Entry.Journal of virology · 2018Article
- Activation of hepatic stellate cells by the ubiquitin C-terminal hydrolase 1 protein secreted from hepatitis C virus-infected hepatocytes.Scientific reports · 2017Article
- Reduction of hepatic fibrosis by overexpression of von Hippel-Lindau protein in experimental models of chronic liver disease.Scientific reports · 2017Article
- L(59) TGF-β LAP degradation products serve as a promising blood biomarker for liver fibrogenesis in mice.Fibrogenesis & tissue repair · 2015Article
- Immunomodulatory effects of transforming growth factor-β in the liver.Hepatobiliary surgery and nutrition · 2014Review
- Recurrent HCV after liver transplantation-mechanisms, assessment and therapy.Nature reviews. Gastroenterology & hepatology · 2014Review
Corrections and comments
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Authors and funding
17 authors at 8 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Viruses sometimes mimic host proteins and hijack the host cell machinery. Hepatitis C virus (HCV) causes liver fibrosis, a process largely mediated by the overexpression of transforming growth factor (TGF)-β and collagen, although the precise underlying mechanism is unknown. Here, we report that HCV non-structural protein 3 (NS3) protease affects the antigenicity and bioactivity of TGF-β2 in (CAGA)9-Luc CCL64 cells and in human hepatic cell lines via binding to TGF-β type I receptor (TβRI). Tumor necrosis factor (TNF)-α facilitates this mechanism by increasing the colocalization of TβRI with NS3 protease on the surface of HCV-infected cells. An anti-NS3 antibody against computationally predicted binding sites for TβRI blocked the TGF-β mimetic activities of NS3 in vitro and attenuated liver fibrosis in HCV-infected chimeric mice. These data suggest that HCV NS3 protease mimics TGF-β2 and functions, at least in part, via directly binding to and activating TβRI, thereby enhancing liver fibrosis.
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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.