ReviewWorld journal of hepatology2015
Recent advances in mouse models of obesity- and nonalcoholic steatohepatitis-associated hepatocarcinogenesis.
Review in World journal of hepatology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.
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Who cites it
38 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Abdominal obesity and digestive system cancer: a systematic review and meta-analysis of prospective studies.BMC public health · 2023Pooled it
- A refined MASH-HCC model identifies macrophage Gadd45b as a key orchestrator of inflammation-driven neoplastic progression.Experimental & molecular medicine · 2026Article
- Reproducibility and Sex Differences in a STZ-High-Fat Diet Model of MASLD and Early Hepatocarcinogenesis.International journal of molecular sciences · 2026Article
- Impaired nitrogenous waste clearance promotes hepatocellular carcinoma.Science advances · 2026Article
- Lipogenesis and MASLD: re-thinking the role of SREBPs.Archives of toxicology · 2025Review
- MARCH8 suppresses hepatocellular carcinoma by promoting SREBP1 degradation and modulating fatty acid de novo synthesis.Cell death & disease · 2025Article
- Mouse Models for the Study of Liver Fibrosis RegressionJournal of clinical and translational hepatology · 2024Review
- Phospholipid isotope tracing suggests β-catenin-driven suppression of phosphatidylcholine metabolism in hepatocellular carcinoma.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2024Article
- Phospholipid isotope tracing reveals β-catenin-driven suppression of phosphatidylcholine metabolism in hepatocellular carcinoma.bioRxiv : the preprint server for biology · 2023Article
- Tale of two systems: the intertwining duality of fibrinolysis and lipoprotein metabolism.Journal of thrombosis and haemostasis : JTH · 2023Review
- Unfolded Protein Response Signaling in Liver Disorders: A 2023 Updated Review.International journal of molecular sciences · 2023Review
- Innate-like T lymphocytes in chronic liver disease.Frontiers in immunology · 2023Review
- Utility of Human Relevant Preclinical Animal Models in Navigating NAFLD to MAFLD Paradigm.International journal of molecular sciences · 2022Review
- IL27 Signaling Serves as an Immunologic Checkpoint for Innate Cytotoxic Cells to Promote Hepatocellular Carcinoma.Cancer discovery · 2022Article
- Inhibiting SCAP/SREBP exacerbates liver injury and carcinogenesis in murine nonalcoholic steatohepatitis.The Journal of clinical investigation · 2022Article
- Immunometabolic factors contributing to obesity-linked hepatocellular carcinoma.Frontiers in cell and developmental biology · 2022Review
- Cell fate analysis of zone 3 hepatocytes in liver injury and tumorigenesis.JHEP reports : innovation in hepatology · 2021Article
- Review
- Hyperlipidemia May Synergize with Hypomethylation in Establishing Trained Immunity and Promoting Inflammation in NASH and NAFLD.Journal of immunology research · 2021Article
- Inside-Out or Outside-In: Choosing the Right Model of Hepatocellular Cancer.Gene expression · 2020Review
Corrections and comments
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Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatocellular carcinoma (HCC) is the fifth most common cancer, and obesity has been established as a risk factor for HCC development. Nonalcoholic steatohepatitis (NASH) is apparently the key link between obesity and hepatocarcinogenesis, and obesity also accelerates HCC development synergistically with other risk factors, such as hepatitis virus infection and alcohol consumption. As an explanation for the pathogenesis of NASH, the so-called "two-hit" theory has been widely accepted, but recently, a better model, the so-called "multiple-hits hypothesis" was proposed, which states that many disease-promoting factors may occur in parallel, rather than consecutively. However, the overall mechanism remains largely unknown. Various cell-cell and organ-organ interactions are involved in the pathogenesis of NASH, and thus appropriate in vivo disease models are essential for a deeper understanding. However, replicating the full spectrum of human NASH has been difficult, as NASH involves obesity, insulin resistance, steatohepatitis, fibrosis, and ultimately HCC, and the lack of an appropriate mouse model has been a considerable barrier to determining the missing links among obesity, NASH, and HCC. In recent years, several innovative mouse models presenting obesity- and NASH-associated HCC have been established by modified diets, chemotoxic agents, genetic manipulation, or a combination of these factors, shedding some light on this complex network and providing new therapeutic strategies. Thus, in this paper, I review the mouse models of obesity- and NASH-associated HCC, especially focusing on recent advances and their clinical relevance.
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