National Institute of Biomedical Innovation, 7-6-8 Saito Asagi, Ibaraki, Osaka 567-0085, Japan.
Evaluation of: Diamond DL, Krasnoselsky AL, Burnum KE et al. Proteome and computational analyses reveal new insights into the mechanisms of hepatitis C virus-mediated liver disease posttransplantation. Hepatology 56(1), 28-38 (2012). HCV is a major cause of chronic liver disease worldwide and is a formidable therapeutic challenge. Recently, Diamond et al. analyzed the proteomic profiles of liver samples from HCV-positive liver transplant recipients, supplemented with an independent metabolite analysis. They used a computational approach, which highlighted the enriched functional themes and topological attributes associated with the protein association network based on their clinical data and suggested a crucial role of oxidative stress in fibrosis progression in HCV infection. Their findings provide new insights into the mechanisms that regulate the progression of HCV-associated liver fibrosis, which may be useful for identification of suitable biomarkers to evaluate the onset and severity of hepatic fibrosis and the development of new therapeutic and anti-HCV strategies.