ReviewFree radical biology & medicine2014
Oxidative stress and hepatic Nox proteins in chronic hepatitis C and hepatocellular carcinoma.
Review in Free radical biology & medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 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
47 citing papers in PubMed, 1 synthesis or guideline pooled it, 84 citations in OpenAlex.
- Global air pollution exposure and hepatocellular carcinoma: a systematic review and meta-analysis of epidemiological studies.BMC public health · 2025Pooled it
- Viral Comorbidities Remodel Host Transcriptome and Redox Signaling in an NADPH Oxidase Isoform-Specific Manner.Viruses · 2026Review
- Unsaponifiable fraction of black Vitis vinifera seed oil attenuates liver cancer progression by targeting apoptosis and key tumor-associated genes: In vitro, in vivo, and in silico studies.Scientific reports · 2026Article
- Molecular mechanisms in MASLD/MASH-related HCC.Hepatology (Baltimore, Md.) · 2025Review
- NOX Family: Regulators of Reactive Oxygen Species Balance in Tumor Cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Review
- Effects of oxidative stress on viral infections: an overview.Npj viruses · 2025Review
- Do oxidized low-density lipoproteins link to extra hepatic manifestations in chronic, non-cirrhotic HCV patients?Metabolism open · 2025Article
- The PI3K/Akt/mTOR Pathway: Immuno-Metabolic Orchestration in IR/MASH-Associated Hepatocellular Carcinoma.International journal of biological sciences · 2025Review
- Metabolism of hepatic stellate cells in chronic liver diseases: emerging molecular and therapeutic interventions.Theranostics · 2025Review
- A literature review of genetics and epigenetics of HCV-related hepatocellular carcinoma: translational impact.Hepatobiliary surgery and nutrition · 2024Review
- Oxidative Stress in Liver Pathophysiology and Disease.Antioxidants (Basel, Switzerland) · 2023Review
- NOX as a Therapeutic Target in Liver Disease.Antioxidants (Basel, Switzerland) · 2022Review
- DNA and RNA oxidative damage in hepatocellular carcinoma patients and mortality during the first year of liver transplantation.World journal of hepatology · 2022Article
- TAZ-induced Cybb contributes to liver tumor formation in non-alcoholic steatohepatitis.Journal of hepatology · 2022Article
- Harnessing reactive oxygen/nitrogen species and inflammation: Nanodrugs for liver injury.Materials today. Bio · 2022Article
- Melatonin is a potential oncostatic agent to inhibit HepG2 cell proliferation through multiple pathways.Heliyon · 2022Article
- The TGF-β/NADPH Oxidases Axis in the Regulation of Liver Cell Biology in Health and Disease.Cells · 2021Review
- Review
- Changes in Glutathione Content in Liver Diseases: An Update.Antioxidants (Basel, Switzerland) · 2021Review
- NADSignal transduction and targeted therapy · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Hepatocellular carcinoma (HCC) is the most common liver cancer and a leading cause of cancer-related mortality in the world. Hepatitis C virus (HCV) is a major etiologic agent of HCC. A majority of HCV infections lead to chronic infection that can progress to cirrhosis and, eventually, HCC and liver failure. A common pathogenic feature present in HCV infection, and other conditions leading to HCC, is oxidative stress. HCV directly increases superoxide and H2O2 formation in hepatocytes by elevating Nox protein expression and sensitizing mitochondria to reactive oxygen species generation while decreasing glutathione. Nitric oxide synthesis and hepatic iron are also elevated. Furthermore, activation of phagocytic NADPH oxidase (Nox) 2 of host immune cells is likely to exacerbate oxidative stress in HCV-infected patients. Key mechanisms of HCC include genome instability, epigenetic regulation, inflammation with chronic tissue injury and sustained cell proliferation, and modulation of cell growth and death. Oxidative stress, or Nox proteins, plays various roles in these mechanisms. Nox proteins also function in hepatic fibrosis, which commonly precedes HCC, and Nox4 elevation by HCV is mediated by transforming growth factor β. This review summarizes mechanisms of oncogenesis by HCV, highlighting the roles of oxidative stress and hepatic Nox enzymes in HCC.
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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.