ReviewWorld journal of gastroenterology2014
Oxidative damage in the progression of chronic liver disease to hepatocellular carcinoma: an intricate pathway.
Review in World journal of gastroenterology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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
40 citing papers in PubMed, 70 citations in OpenAlex.
- rt269I Type of Hepatitis B Virus (HBV) Leads to HBV e Antigen Negative Infections and Liver Disease Progression via Mitochondrial Stress Mediated Type I Interferon Production in Chronic Patients With Genotype C Infections.Frontiers in immunology · 2019Trial
- Article
- Apigenin attenuates obesity-associated hepatic dysfunction and fibrosis in rats: an integrated biochemical, histological, and ex vivo dielectric study.BMC pharmacology & toxicology · 2026Article
- Plant-Derived Bioactive Compounds in Inflammation-Related Cancers: Mechanisms and Therapeutic Potential.Plants (Basel, Switzerland) · 2026Review
- Therapeutic Potential of Mesenchymal Stem Cell-Derived Extracellular Vesicles in Digestive System Tumors: Modulating the Chronic Inflammatory Microenvironment.International journal of nanomedicine · 2026Review
- SIRT1-Mediated Redox and Senescence Regulation in Cancer: Mechanisms and Therapeutic Implications.Antioxidants (Basel, Switzerland) · 2025Review
- The protective effects and mechanism of myricetin in liver diseases (Review).Molecular medicine reports · 2025Review
- The role and mechanism of selenium in the prevention and progression of hepatocellular carcinoma.Frontiers in oncology · 2025Review
- Mitochondrial dysfunction: A promising therapeutic target for liver diseases.Genes & diseases · 2024Review
- Investigating the association between blood metabolites and telomere length: A mendelian randomization study.PloS one · 2024Article
- The Roles of NFR2-Regulated Oxidative Stress and Mitochondrial Quality Control in Chronic Liver Diseases.Antioxidants (Basel, Switzerland) · 2023Review
- From liver fibrosis to hepatocarcinogenesis: Role of excessive liver HBioactive materials · 2023Article
- Eicosapentaenoic acid loaded silica nanoemulsion attenuates hepatic inflammation through the enhancement of cell membrane components.Biological procedures online · 2022Article
- Article
- Two Faces of Neutrophils in Liver Disease Development and Progression.Hepatology (Baltimore, Md.) · 2021Review
- Natural Polyphenols in Metabolic Syndrome: Protective Mechanisms and Clinical Applications.International journal of molecular sciences · 2021Review
- Critical signaling pathways governing hepatocellular carcinoma behavior; small molecule-based approaches.Cancer cell international · 2021Review
- The Impact of Hepatitis C Virus Genotypes on Oxidative Stress Markers and Catalase Activity.Oxidative medicine and cellular longevity · 2021Article
- Dietary vitamin D ameliorates hepatic oxidative stress and inflammatory effects of diethylnitrosamine in rats.Heliyon · 2020Article
- Effect of HBx on inflammation and mitochondrial oxidative stress in mouse hepatocytes.Oncology letters · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The histo-pathologic and molecular mechanisms leading to initiation and progression of hepatocellular carcinoma (HCC) are still ill-defined; however, there is increasing evidence that the gradual accumulation of mutations, genetic and epigenetic changes which occur in preneoplastic hepatocytes results in the development of dysplastic foci, nodules, and finally, overt HCC. As well as many other neoplasias, liver cancer is considered an "inflammatory cancer", arising from a context of inflammation, and characterized by inflammation-related mechanisms that favor tumor cell survival, proliferation, and invasion. Molecular mechanisms that link inflammation and neoplasia have been widely investigated, and it has been well established that inflammatory cells recruited at these sites with ongoing inflammatory activity release chemokines that enhance the production of reactive oxygen species. The latter, in turn, probably have a major pathogenic role in the continuum starting from hepatitis followed by chronic inflammation, and ultimately leading to cancer. The relationship amongst chronic liver injury, free radical production, and development of HCC is explored in the present review, particularly in the light of the complex network that involves oxidative DNA damage, cytokine synthesis, telomere dysfunction, and microRNA regulation.
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.