ReviewInternational journal of molecular sciences2024
Fibrosis and Hepatocarcinogenesis: Role of Gene-Environment Interactions in Liver Disease Progression.
Review in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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.
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.
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Who cites it
15 citing papers in PubMed.
- Engineered protein nanoclusters reduce liver fibrosis and hepatocellular carcinoma in mice models.Bioactive materials · 2026Article
- Article
- Nanozyme for precision treatment of hepatocellular carcinoma.Materials today. Bio · 2026Review
- Therapeutic Strategies for Hepatocellular Carcinoma: Current Advances and Future Perspectives.Vaccines · 2026Review
- Inflammation in hepatocellular carcinoma progression: a "Single Wick, dual interwoven strands" regulatory framework.Frontiers in immunology · 2026Review
- Vitisin A inhibits liver fibrosis by promoting Nrf2/HO-1 pathway and inhibiting Cuproptosis.Scientific reports · 2025Article
- Effects of the Polar Fraction ofInternational journal of molecular sciences · 2025Article
- Present and Future Perspectives in the Treatment of Liver Fibrosis.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Clinical and Endoscopic-Histological Features of Multifocal and Corpus-Restricted Atrophic Gastritis Patients With Non-Cardia Gastric Cancer or Dysplasia: A Multicenter, Cross-Sectional Study.Clinical and translational gastroenterology · 2025Article
- Pantothenic acid ameliorates hepatic fibrosis by targeting IGFBP6 to regulate the TGF-β/SMADs pathway.Communications biology · 2025Article
- Long noncoding RNA MEG3: an active player in fibrosis.Pharmacological reports : PR · 2025Review
- Correlation of sarcopenia with progression of liver fibrosis in patients with metabolic dysfunction-associated steatotic liver disease: a study from two cohorts in China and the United States.Nutrition journal · 2025Article
- Dihydroartemisinin: A Promising Therapeutic Agent Against the Hepatitis-to-Hepatocellular Carcinoma Cascade.Drug design, development and therapy · 2025Review
- Prognostic Significance of Preoperative Inflammatory and Liver Fibrosis Markers in Hepatocellular Carcinoma.Journal of inflammation research · 2025Article
- The burden of cancer in metabolic dysfunction-associated steatotic liver disease.Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologieReview
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The liver is a complex organ that performs vital functions in the body. Despite its extraordinary regenerative capacity compared to other organs, exposure to chemical, infectious, metabolic and immunologic insults and toxins renders the liver vulnerable to inflammation, degeneration and fibrosis. Abnormal wound healing response mediated by aberrant signaling pathways causes chronic activation of hepatic stellate cells (HSCs) and excessive accumulation of extracellular matrix (ECM), leading to hepatic fibrosis and cirrhosis. Fibrosis plays a key role in liver carcinogenesis. Once thought to be irreversible, recent clinical studies show that hepatic fibrosis can be reversed, even in the advanced stage. Experimental evidence shows that removal of the insult or injury can inactivate HSCs and reduce the inflammatory response, eventually leading to activation of fibrolysis and degradation of ECM. Thus, it is critical to understand the role of gene-environment interactions in the context of liver fibrosis progression and regression in order to identify specific therapeutic targets for optimized treatment to induce fibrosis regression, prevent HCC development and, ultimately, improve the clinical outcome.
Indexed as
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Registered trials
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