ArticlePloS one2016
Protective Role of Sirtuin3 (SIRT3) in Oxidative Stress Mediated by Hepatitis B Virus X Protein Expression.
Article in PloS one, 2016. 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
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The trial behind it
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Who cites it
48 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.
- Pooled it
- Combining antiviral therapy with cancer treatment in HBV-associated HCC: A translational approach.Virus research · 2026Review
- HBx Enhances the Nrf2/ARE-dependent Antioxidant Response by Promoting Nuclear Export and Downregulation of Bach1.The Kobe journal of medical sciences · 2026Article
- CircRNA-encoded protein fine-tunes ROS homeostasis and engages conserved JAK-STAT antiviral defenses inJournal of virology · 2026Article
- The Role of Integrated HBV DNA in the Quest for a Cure in HIV/HBV co-infection.Current HIV/AIDS reports · 2025Review
- Effects of oxidative stress on viral infections: an overview.Npj viruses · 2025Review
- Oxidative Stress in Brain Function.Antioxidants (Basel, Switzerland) · 2025Review
- Metformin Activation of Sirtuin 3 Signaling Regulates Mitochondrial Function Improves Diabetes-Associated Cognitive Impairment.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025Article
- SIRT3, a New Hope in Liver Diseases from Pathogenic Mechanisms to Therapeutic Strategies.Current pharmaceutical biotechnology · 2025Review
- Inhibition of BRD4 activates the AKT-SIRT3 signaling pathway to suppress apoptosis and attenuate hyperoxia-induced lung injury.Frontiers in bioengineering and biotechnology · 2025Article
- Hepatitis B Virus X Protein Induces Reactive Oxygen Species Generation via Activation of p53 in Human Hepatoma Cells.Biomolecules · 2024Article
- Reactive Oxygen Species Induction by Hepatitis B Virus: Implications for Viral Replication in p53-Positive Human Hepatoma Cells.International journal of molecular sciences · 2024Article
- Hydrogen Peroxide Inhibits Hepatitis B Virus Replication by Downregulating HBx Levels via Siah-1-Mediated Proteasomal Degradation in Human Hepatoma Cells.International journal of molecular sciences · 2023Article
- The Role of Glutathione in Selected Viral Diseases.Antioxidants (Basel, Switzerland) · 2023Review
- Decoding the multifaceted interventions between human sirtuin 2 and dynamic hepatitis B viral proteins to confirm their roles in HBV replication.Frontiers in cellular and infection microbiology · 2023Review
- Prognostic value of plasma level of superoxide dismutase in HBV-related acute-on-chronic liver failure.BMC gastroenterology · 2022Article
- Oxidative Stress in Chronic Hepatitis B-An Update.Microorganisms · 2022Review
- SIRT3 regulates bronchial epithelium apoptosis and aggravates airway inflammation in asthma.Molecular medicine reports · 2022Article
- The mTOR/PGC-1α/SIRT3 Pathway Drives Reductive Glutamine Metabolism to Reduce Oxidative Stress Caused by ISKNV in CPB Cells.Microbiology spectrum · 2022Article
- The Effect of Antiretroviral Therapy on SIRT1, SIRT3 and SIRT6 Expression in HIV-Infected Patients.Molecules (Basel, Switzerland) · 2022Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND/
aimThe hepatitis B virus (HBV) infection is accompanied by the induction of oxidative stress, especially mediated by HBV X protein (HBx). Oxidative stress has been implicated in a series of pathological states, such as DNA damage, cell survival and apoptosis. However, the host factor by which cells protect themselves under this oxidative stress is poorly understood. METHODOLOGY/PRINCIPAL
findingsIn this study, we first confirmed that HBV infection significantly induced oxidative stress. Moreover, viral protein HBx plays a major role in the oxidative stress induced by HBV. Importantly, we found that mitochondrial protein SIRT3 overexpression could decrease reactive oxygen species (ROS) induced by HBx while SIRT3 knockdown increased HBx-induced ROS. Importantly, SIRT3 overexpression abolished oxidative damage of HBx-expressing cells as evidenced by γH2AX and AP sites measurements. In contrast, SIRT3 knockdown promoted HBx-induced oxidative damage. In addition, we also observed that oxidant H2O2 markedly promoted HBV replication while the antioxidant N-acetyl-L-cysteine (NAC) inhibited HBV replication. Significantly, SIRT3 overexpression inhibited HBV replication by reducing cellular ROS level. CONCLUSIONS/SIGNIFICANCE: Collectively, these data suggest HBx expression induces oxidative stress, which promotes cellular oxidative damage and viral replication during HBV pathogenesis. Mitochondrial protein SIRT3 protected HBx expressing-cells from oxidative damage and inhibited HBV replication possibly by decreased cellular ROS level. These studies shed new light on the physiological significance of SIRT3 on HBx-induced oxidative stress, which can contribute to the liver pathogenesis.
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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.