HCV (hepatitis C virus) represents one of the major health problems worldwide, as almost 170 million people are infected and most of these develop a chronic disease, often with the progression to cirrhosis and its complications. In the present issue of Clinical Science, Iwata and co-workers report an association between a variant of a gene regulating bile acid levels, ABCB11 1331T>C (where ABCB11 encodes ATP-binding cassette, subfamily B, member 11), and the progression to cirrhosis in patients with HCV, but not in fatty liver patients. They correlate this genetic variant with increased serum bile acid levels as a marker of cholestasis. These findings have important implications for researchers working to dissect the molecular mechanisms underlying liver fibrogenesis and disease progression; however, the implications for clinical hepatologists are less immediate.
- Bile acid transport
- Bile salt export pump (BSEP)
- Farnesoid X receptor (FXR)
- Non-alcoholic fatty liver disease (NAFLD)
- Single nucleotide polymorphism
- Viral hepatitis
ASJC Scopus subject areas