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• W2904657528 abstract "Nonalcoholic steatohepatitis ( NASH ) is a common cause of liver cirrhosis and hepatocellular carcinoma ( HCC ). However, effective therapeutic strategies for preventing and treating NASH ‐mediated liver cirrhosis and HCC are lacking. Cholesterol is closely associated with vascular endothelial growth factor ( VEGF ), a key factor that promotes HCC . Recent reports have demonstrated that statins could prevent HCC development. In contrast, we have little information on ezetimibe, an inhibitor of cholesterol absorption, in regards to the prevention of NASH ‐related liver cirrhosis and HCC . In the present study, a steatohepatitis‐related HCC model, hepatocyte‐specific phosphatase and tensin homolog ( Pten )‐deficient ( Pten Δhep ) mice were fed a high‐fat ( HF ) diet with/without ezetimibe. In the standard‐diet group, ezetimibe did not reduce the development of liver tumors in Pten Δhep mice, in which the increase of serum cholesterol levels was mild. Feeding of a HF diet increased serum cholesterol levels markedly and subsequently increased serum levels of VEGF , a crucial component of angiogenesis. The HF diet increased the number of VEGF ‐positive cells and vascular endothelial cells in the tumors of Pten Δhep mice. Kupffer cells, macrophages in the liver, increased VEGF expression in response to fat overload. Ezetimibe treatment lowered cholesterol levels and these angiogenetic processes. As a result, ezetimibe also suppressed inflammation, liver fibrosis and tumor growth in Pten Δhep mice on the HF diet. Tumor cells were highly proliferative with HF ‐diet feeding, which was inhibited by ezetimibe. In conclusion, ezetimibe suppressed development of liver tumors by inhibiting angiogenesis in Pten Δhep mice with hypercholesterolemia." @default.
• W2904657528 created "2018-12-22" @default.
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• W2904657528 date "2019-01-09" @default.
• W2904657528 modified "2023-10-16" @default.
• W2904657528 title "Ezetimibe suppresses development of liver tumors by inhibiting angiogenesis in mice fed a high‐fat diet" @default.
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• W2904657528 doi "https://doi.org/10.1111/cas.13902" @default.
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