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Uptake of Gd-EOB-DTPA in HCC is determined by expression of OATP1B3 rather than by tumor differentiation or bile production.

The origin of fibrogenic cells in liver fibrosis remains controversial. We assessed the emerging concept that hepatocytes contribute to production of extracellular matrix (ECM) in liver fibrosis through epithelial-mesenchymal transition (EMT). We bred triple transgenic mice expressing ROSA26 stop ␤-galactosidase (␤-gal), albumin Cre, and collagen ␣1 (

Chronic hepatitis C is characterized by iron accumulation in the liver, and excessive iron is hepatotoxic. However, the mechanism by which hepatitis C virus (HCV) regulates iron metabolism is poorly understood. Hepcidin plays a pivotal role as a negative regulator of iron absorption. The aim of the current study was to elucidate the mechanisms that govern hepcidin expression by HCV. Huh 7 cells, Huh7. Iron is an essential metal that functions as a component of oxygen-carrying proteins and of redox enzymes in cellular metabolism. However, excessive iron evokes inflammatory cytokines, reactive oxygen species (ROS), and fibrosis by activating inflammatory cells and hepatic stellate cells. 2,3 Furthermore, ROS causes oxidative damage to lipids, proteins, and nucleic acids. 4 Excessive iron is a presumptive factor that contributes to insulin resistance, steatosis, liver fibrosis, and hepatic carcinogenesis, which are common sequelae of chronic HCV infection.Chronic HCV infection is also characterized by iron deposition in the liver, which contributes to liver injury. 4,5 Withdrawal of iron by phlebotomy improves liver