ArticleFEBS open bio2018
A critical role of hepatitis B virus polymerase in cirrhosis, hepatocellular carcinoma, and steatosis.
Article in FEBS open bio, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
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Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- Targeting ferroptosis induction via nanomaterials in hepatocellular carcinoma: an insight into mechanism and therapeutic potential.Journal of nanobiotechnology · 2026Review
- Prevalence and Molecular Characterization of Chronic and Occult Hepatitis B Virus Infection Among Pregnant Women in St. Petersburg, Russia.International journal of molecular sciences · 2025Article
- Mechanisms of hepatocellular carcinoma and cirrhosis development in concurrent steatotic liver disease and chronic hepatitis B.Clinical and molecular hepatology · 2025Review
- Article
- Preclinical Models of Hepatocellular Carcinoma: Current Utility, Limitations, and Challenges.Biomedicines · 2024Review
- An overview of mouse models of hepatocellular carcinoma.Infectious agents and cancer · 2023Review
- The role of hepatitis B virus genome variations in HBV-related HCC: effects on host signaling pathways.Frontiers in microbiology · 2023Review
- Roborovski hamsterVirulence · 2021Article
- CNOT7 depletion reverses natural killer cell resistance by modulating the tumor immune microenvironment of hepatocellular carcinoma.FEBS open bio · 2020Article
- Article
- Molecular Mechanisms Driving Progression of Liver Cirrhosis towards Hepatocellular Carcinoma in Chronic Hepatitis B and C Infections: A Review.International journal of molecular sciences · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatitis B is one of the most common infectious diseases in the world; more than 350 million people are carriers of hepatitis B virus (HBV). Chronic HBV infection (CHB) leads to liver diseases such as cirrhosis, hepatocellular carcinoma (HCC), and steatosis. Despite its seriousness in terms of public health, the pathogenic mechanism of how CHB leads to liver diseases, especially cirrhosis and steatosis, remains unclear. We studied the role of HBV polymerase (HBp) reverse transcriptase (RT) activity in association with the pathogenesis of liver diseases in CHB by developing transgenic mice expressing HBp or the RT domain of HBp. Thorough pathological, serological, and histological analyses of the transgenic mice, as well as mechanistic studies, were conducted. All of the transgenic mice expressing RT in their livers developed early cirrhosis with steatosis by 18 months of age, and 10% developed HCC. The RT activity of HBp stimulates coordinated proapoptotic and proinflammatory responses involving the caspase-9, caspase-3, and caspase-1 pathways that might lead to the development of cirrhosis, HCC, and steatosis. The animal model described here should prove useful for elucidating the molecular events in the CHB-induced liver diseases.
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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.