The identification of a gene contributing to the proliferation of fibrous tissue in the liver has been reported in a study in the August issue of Nature Genetics. Chronic liver diseases lead to such liver fibrosis, involving the degradation of normal tissue and replacement with fibrous tissue (scarring), and are the 10th leading cause of mortality in the United States and the 16th globally. Infection with hepatitis C virus (HCV) is one of the frequent causes of chronic liver disease, with approximately 25% of individuals with chronic HCV developing liver fibrosis within 30 years after infection.

Frank Lammert and colleagues first identified the gene (complement factor 5) associated with liver fibrosis in mice, and then confirmed this association in a human population of individuals positive for hepatitis C virus infection. Complement factor 5, which has also been associated with susceptibility to asthma, may contribute to liver fibrogenesis by promoting inflammation or tissue remodeling, although its precise mechanism of action is not yet known. In mice, introducing inhibitors of this protein reduced the extent of liver fibrosis. This suggests potential drug targets reducing, or at least delaying, progression of liver fibrosis in individuals with chronic hepatitis C infection and chronic liver diseases.

[5] Inversion-induced disruption of the Hoxd cluster leads to the partition of regulatory landscapes

DOI: 10.1038/ng1597 DOI: 10.1038/ng1599

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nature

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alphagalileo