ArticleMedical molecular morphology2013
A murine model for non-alcoholic steatohepatitis showing evidence of association between diabetes and hepatocellular carcinoma.
Article in Medical molecular morphology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 217 papers.
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217 citing papers in PubMed, 339 citations in OpenAlex.
- Alcohol reshapes liver zonal plasticity and immune-metabolic reprogramming in metabolic-syndrome associated hepatocellular carcinoma.Nature communications · 2026Article
- NucVerse3D: generalizable 3D nuclear instance segmentation across heterogeneous microscopy modalities.Scientific reports · 2026Article
- Development and characterization of dietary models of MASLD with portal hypertension and liver fibrosis in rats.Lab animal · 2026Article
- Comparison and Characteristics of MASLD Mouse Models.Biomedicines · 2026Review
- ATP synthase is a promising target for identifying activated and non-activated adipose tissues.Nature communications · 2026Article
- Constitutive AMPK activation prevents hepatocellular carcinoma development through inhibition of HNF4α activity.Science advances · 2026Article
- Metabolic dysfunction-associated steatotic liver disease and steatohepatitis-associated hepatocarcinoma preclinical models.Nature reviews. Gastroenterology & hepatology · 2026Review
- Reproducibility and Sex Differences in a STZ-High-Fat Diet Model of MASLD and Early Hepatocarcinogenesis.International journal of molecular sciences · 2026Article
- Cholesterol-rich diet exacerbates steatohepatitis in the STAM mouse model.Scientific reports · 2026Article
- Oncogenic function and transcriptional dynamics of MYCN in liver tumorigenesis.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Adipose tissue-derived MFG-E8 promotes hepatic inflammation and fibrosis through macrophage activation in a mouse MASH model.npj metabolic health and disease · 2026Article
- Time-Restricted Feeding Is Not Effective in Modulating Fibrosis in a Male MASH Model.Journal of biological rhythms · 2026Article
- A Mouse in vivo Model Mimicking MASH-Related HCC Pathogenesis.Journal of hepatocellular carcinoma · 2026Article
- Life history enlightened therapies: cell cycle mapping to identify molecular targets to prevent hepatocellular carcinoma.Evolution, medicine, and public health · 2026Article
- Targeting the hepatic circadian clock concomitant with tyrosine kinase inhibition reverses late-stage hepatocellular carcinoma.Cell reports · 2025Article
- Elevated miR-34a induced by lipotoxicity and inflammation mediates pathophysiological communication between hepatocytes and hepatic stellate cells in liver fibrosis.Genes & diseases · 2025Article
- Article
- Targeted inhibition of hepatic de novo ceramide synthesis ameliorates MASH.Science advances · 2025Article
- Navigating liver cancer with mouse models: a comprehensive overview of HCC experimental systems.Journal of liver cancer · 2025Article
- Decoding the Liver-Heart Axis in Cardiometabolic Diseases.Circulation research · 2025Review
157 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatocellular carcinoma (HCC) is the third most common cause of cancer-related deaths. In addition to hepatitis viral infections, several cohort studies have shown that diabetes mellitus is a risk factor of HCC, making the incidence alarming high. However, it has not been demonstrated directly how diabetes develops to HCC, because of its difficulty to follow changes of liver histology in diabetic populations. Here, we report that non-alcoholic steatohepatitis (NASH) is pivotal to link diabetes with HCC by establishing a novel, reproducible NASH-HCC model in mice. Neonatal male mice exposed to low-dose streptozotocin (STZ) developed liver steatosis with diabetes 1 week after feeding high-fat diet (HFD). Continuous HFD decreased hepatic fat deposit whilst increased lobular inflammation with foam cell-like macrophages, showing NASH pathology. In parallel with decreased phagocytosis of macrophages, fibroblasts accumulated to form "chicken-wired" fibrosis. All mice developed multiple HCC later. Female mice treated with STZ-HFD and male mice treated with STZ alone showed diabetes but never developed HCC by the absence of NASH-based fibrosis. Thus, the present study provides the evidence in novel mouse model that NASH-based fibrosis is an essential histological process for diabetic populations to accelerate the development of HCC.
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