ArticleOxidative medicine and cellular longevity2016
Hepatitis C Virus NS5A Protein Triggers Oxidative Stress by Inducing NADPH Oxidases 1 and 4 and Cytochrome P450 2E1.
Article in Oxidative medicine and cellular longevity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 59 citations in OpenAlex.
- HBV/HCV coinfection and anti-tuberculosis drug-induced liver injury: from risk assessment and exploration of mechanisms to preventive considerations.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2026Review
- Viral Comorbidities Remodel Host Transcriptome and Redox Signaling in an NADPH Oxidase Isoform-Specific Manner.Viruses · 2026Review
- The spatiotemporal heterogeneity of reactive oxygen species in the malignant transformation of viral hepatitis to hepatocellular carcinoma: a new insight.Cellular & molecular biology letters · 2025Review
- Defence Warriors: Exploring the crosstalk between polyamines and oxidative stress during microbial pathogenesis.Redox biology · 2025Review
- Drug-Induced Liver Injury in Patients With Chronic Liver Disease.Liver international : official journal of the International Association for the Study of the Liver · 2025Review
- Endoplasmic reticulum oxidoreductin 1α as a potential therapeutic target in diseases: from oxidative protein folding to pathophysiological mechanisms.Frontiers in pharmacology · 2025Review
- Inflammatory Response in the Pathogenesis and Treatment of Hepatocellular Carcinoma: A Double-Edged Weapon.International journal of molecular sciences · 2024Review
- Impact of Human Adenovirus 36 on Embryonated Chicken Eggs: Insights into Growth Mechanisms.International journal of molecular sciences · 2024Article
- The emerging role of oxidative stress in inflammatory bowel disease.Frontiers in endocrinology · 2024Review
- Review
- Transcriptome Analysis of Redox Systems and Polyamine Metabolic Pathway in Hepatoma and Non-Tumor Hepatocyte-like Cells.Biomolecules · 2023Article
- Hepatitis Delta Virus Antigens Trigger Oxidative Stress, Activate Antioxidant Nrf2/ARE Pathway, and Induce Unfolded Protein Response.Antioxidants (Basel, Switzerland) · 2023Article
- Eicosanoids and other oxylipins in liver injury, inflammation and liver cancer development.Frontiers in physiology · 2023Review
- Clinical Research Progress of Small Molecule Compounds Targeting Nrf2 for Treating Inflammation-Related Diseases.Antioxidants (Basel, Switzerland) · 2022Review
- Molecular signature of postmortem lung tissue from COVID-19 patients suggests distinct trajectories driving mortality.Disease models & mechanisms · 2022Article
- Signaling Induced by Chronic Viral Hepatitis: Dependence and Consequences.International journal of molecular sciences · 2022Review
- The Nrf2 Pathway in Liver Diseases.Frontiers in cell and developmental biology · 2022Review
- Non-cirrhotic hepatocellular carcinoma in chronic viral hepatitis: Current insights and advancements.World journal of gastroenterology · 2021Review
- The Impact of Hepatitis C Virus Genotypes on Oxidative Stress Markers and Catalase Activity.Oxidative medicine and cellular longevity · 2021Article
- Hepatitis C virus and carpal tunnel syndrome in hemodialysis patients: a single center cross-sectional study.Renal failure · 2020Observational
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Replication of hepatitis C virus (HCV) is associated with the induction of oxidative stress, which is thought to play a major role in various liver pathologies associated with chronic hepatitis C. NS5A protein of the virus is one of the two key viral proteins that are known to trigger production of reactive oxygen species (ROS). To date it has been considered that NS5A induces oxidative stress by altering calcium homeostasis. Herein we show that NS5A-induced oxidative stress was only moderately inhibited by the intracellular calcium chelator BAPTA-AM and not at all inhibited by the drug that blocks the Ca(2+) flux from ER to mitochondria. Furthermore, ROS production was not accompanied by induction of ER oxidoreductins (Ero1), H2O2-producing enzymes that are implicated in the regulation of calcium fluxes. Instead, we found that NS5A contributes to ROS production by activating expression of NADPH oxidases 1 and 4 as well as cytochrome P450 2E1. These effects were mediated by domain I of NS5A protein. NOX1 and NOX4 induction was mediated by enhanced production of transforming growth factor β1 (TGFβ1). Thus, our data show that NS5A protein induces oxidative stress by several multistep mechanisms.
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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.