ReviewViruses2013
Hepatitis C virus-induced mitochondrial dysfunctions.
Review in Viruses, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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
34 citing papers in PubMed, 68 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
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- Bioinspired exosome-SiOTheranostics · 2025Article
- Hepatitis B Virus and Hepatitis C Virus Affect Mitochondrial Function Through Different Metabolic Pathways, Explaining Virus-Specific Clinical Features of Chronic Hepatitis.The Journal of infectious diseases · 2024Article
- Role of Divalent Cations in Infections in Host-Pathogen Interaction.International journal of molecular sciences · 2024Review
- Targeting mitochondrial quality control: new therapeutic strategies for major diseases.Military Medical Research · 2024Review
- ATAD1 inhibits hepatitis C virus infection by removing the viral TA-protein NS5B from mitochondria.EMBO reports · 2023Article
- Anti-inflammatory and antifibrotic effects of CBP/β-catenin inhibitor for hepatocytes: small molecular inhibitor, OP-724 possibly improves liver function.Medical molecular morphology · 2023Article
- Review
- Hepatitis C Virus-Related Central and Peripheral Nervous System Disorders.Brain sciences · 2021Review
- Anti-diabetics and antimicrobials: Harmony of mutual interplay.World journal of diabetes · 2021Review
- Dysregulation of host cell calcium signaling during viral infections: Emerging paradigm with high clinical relevance.Molecular aspects of medicine · 2021Review
- Traditional Chinese Medicine and Western Medicine Share Similar Philosophical Approaches to Fight COVID-19.Aging and disease · 2021Article
- Oxidative Stress Induces Mitochondrial Compromise in CD4 T Cells From Chronically HCV-Infected Individuals.Frontiers in immunology · 2021Article
- Porcine deltacoronavirus (PDCoV) modulates calcium influx to favor viral replication.Virology · 2020Article
- European mitochondrial haplogroups predict liver-related outcomes in patients coinfected with HIV and HCV: a retrospective study.Journal of translational medicine · 2019Article
- Article
- Mitochondrial electron transport chain complex III sustains hepatitis E virus replication and represents an antiviral target.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Hepatitis C: From inflammatory pathogenesis to anti-inflammatory/hepatoprotective therapy.World journal of gastroenterology · 2018Review
- Bicyclol Attenuates Liver Inflammation Induced by Infection of Hepatitis C VirusFrontiers in pharmacology · 2018Article
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 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic hepatitis C is characterized by metabolic disorders and a microenvironment in the liver dominated by oxidative stress, inflammation and regeneration processes that lead in the long term to hepatocellular carcinoma. Many lines of evidence suggest that mitochondrial dysfunctions, including modification of metabolic fluxes, generation and elimination of oxidative stress, Ca2+ signaling and apoptosis, play a central role in these processes. However, how these dysfunctions are induced by the virus and whether they play a role in disease progression and neoplastic transformation remains to be determined. Most in vitro studies performed so far have shown that several of the hepatitis C virus (HCV) proteins localize to mitochondria, but the consequences of these interactions on mitochondrial functions remain contradictory, probably due to the use of artificial expression and replication systems. In vivo studies are hampered by the fact that innate and adaptive immune responses will overlay mitochondrial dysfunctions induced directly in the hepatocyte by HCV. Thus, the molecular aspects underlying HCV-induced mitochondrial dysfunctions and their roles in viral replication and the associated pathology need yet to be confirmed in the context of productively replicating virus and physiologically relevant in vitro and in vivo model systems.
Indexed as
Identifiers
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.