ReviewOxidative medicine and cellular longevity2013
Mitochondrial dysfunctions and altered metals homeostasis: new weapons to counteract HCV-related oxidative stress.
Review in Oxidative medicine and cellular longevity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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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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.
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Who cites it
17 citing papers in PubMed, 29 citations in OpenAlex.
- Preoperative Zinc Deficiency as a Novel Prognostic Predictor for Postoperative Recurrence in Hepatocellular Carcinoma.Nutrients · 2026Article
- Oncoviruses at the Crossroads of Ageing and Cancer: Molecular Mechanisms and Key Signalling Pathways.Reviews in medical virology · 2026Review
- The pivotal role of mitochondria in the pathogenesis and treatment of liver failure: a comprehensive review.Molecular and cellular biochemistry · 2026Review
- Hepatitis C virus alters the morphology and function of peroxisomes.Frontiers in microbiology · 2023Article
- Oxidative stress, immunological and cellular hypoxia biomarkers in hepatitis C treatment-naïve and cirrhotic patients.Archives of medical science : AMS · 2021Article
- Mitochondria in the biology, pathogenesis, and treatment of hepatitis virus infections.Reviews in medical virology · 2019Review
- Peroxisomes and Innate Immunity: Antiviral Response and Beyond.International journal of molecular sciences · 2019Review
- New Insights in the Pathogenesis of HPV Infection and the Associated Carcinogenic Processes: The Role of Chronic Inflammation and Oxidative Stress.Journal of immunology research · 2018Review
- Hepatoprotective Role of Hydrangea macrophylla against Sodium Arsenite-Induced Mitochondrial-Dependent Oxidative Stress via the Inhibition of MAPK/Caspase-3 Pathways.International journal of molecular sciences · 2017Article
- The Paradoxical Effects of Different Hepatitis C Viral Loads on Host DNA Damage and Repair Abilities.PloS one · 2017Article
- HCV-Induced Oxidative Stress: Battlefield-Winning Strategy.Oxidative medicine and cellular longevity · 2016Review
- An overview on therapeutics attenuating amyloid β level in Alzheimer's disease: targeting neurotransmission, inflammation, oxidative stress and enhanced cholesterol levels.American journal of translational research · 2016Review
- Sulforaphane Suppresses Hepatitis C Virus Replication by Up-Regulating Heme Oxygenase-1 Expression through PI3K/Nrf2 Pathway.PloS one · 2016Article
- Oxidative Stress in the Healthy and Wounded Hepatocyte: A Cellular Organelles Perspective.Oxidative medicine and cellular longevity · 2016Review
- Altered metal metabolism in patients with HCV-related cirrhosis and hepatic encephalopathy.Metabolic brain disease · 2015Article
- Mitochondrial Redox Dysfunction and Environmental Exposures.Antioxidants & redox signaling · 2015Review
- Cellular and molecular mechanisms in the pathogenesis of liver fibrosis: An update.World journal of gastroenterology · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The hepatitis C virus (HCV) infection produces several pathological effects in host organism through a wide number of molecular/metabolic pathways. Today it is worldwide accepted that oxidative stress actively participates in HCV pathology, even if the antioxidant therapies adopted until now were scarcely effective. HCV causes oxidative stress by a variety of processes, such as activation of prooxidant enzymes, weakening of antioxidant defenses, organelle damage, and metals unbalance. A focal point, in HCV-related oxidative stress onset, is the mitochondrial failure. These organelles, known to be the "power plants" of cells, have a central role in energy production, metabolism, and metals homeostasis, mainly copper and iron. Furthermore, mitochondria are direct viral targets, because many HCV proteins associate with them. They are the main intracellular free radicals producers and targets. Mitochondrial dysfunctions play a key role in the metal imbalance. This event, today overlooked, is involved in oxidative stress exacerbation and may play a role in HCV life cycle. In this review, we summarize the role of mitochondria and metals in HCV-related oxidative stress, highlighting the need to consider their deregulation in the HCV-related liver damage and in the antiviral management of patients.
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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.