Tomonori Aoyama, Yong‐Han Paik, Sumio Watanabe, Benoît Laleu, Francesca Gaggini, Laetitia Fioraso‐Cartier, Sophie Molango, Freddy Heitz, Cédric Merlot, Cédric Szyndralewiez, Patrick Page, David A. Brenner – 14 July 2012 – Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX) generates reactive oxygen species (ROS) in hepatic stellate cells (HSCs) during liver fibrosis. In response to fibrogenic agonists, such as angiotensin II (Ang II), the NOX1 components form an active complex, including Ras‐related botulinum toxin substrate 1 (Rac1).

Michael E. Mullins, Evan Schwarz – 14 July 2012

Massimo Puoti, Maria Cristina Moioli, Roberto Rossotti, Giovanna Travi, Raffaele Bruno – 14 July 2012

Shaoyong Li, Lianne E.M. Vriend, Imad A. Nasser, Yury Popov, Nezam H. Afdhal, Margaret J. Koziel, Detlef Schuppan, Mark A. Exley, Nadia Alatrakchi – 14 July 2012 – Hepatitis C virus (HCV)‐specific immune effector responses can cause liver damage in chronic infection. Hepatic stellate cells (HSC) are the main effectors of liver fibrosis. TGFβ, produced by HCV‐specific CD8+ T cells, is a key regulatory cytokine modulating HCV‐specific effector T cells.

Christopher H. Remien, Frederick R. Adler, Terry D. Box, Lindsey Waddoups, Norman L. Sussman – 14 July 2012

Drren G. Craig, Kenneth J. Simpson – 14 July 2012

Brent A. Neuschwander‐Tetri, David Q.‐H. Wang – 14 July 2012

Ching‐Lung Lai, Man‐Fung Yuen – 13 July 2012 – Chronic hepatitis B (CHB) infection is the major cause of hepatocellular carcinoma (HCC). Primary prevention of hepatitis B infection by vaccination is effective in reducing the incidence of HCC. In persons with CHB infection, the two accepted treatment modalities are interferon alpha (IFN‐α) given subcutaneously for a limited period and nucleoside/nucleotide analogs given orally on a long‐term basis. These treatments are effective in suppressing viral activity and improving disease markers in short‐term studies.

Andrew Aronsohn, Donald Jensen – 13 July 2012

Mei Huang, Rui Sun, Haiming Wei, Zhigang Tian – 13 July 2012 – NKG2D activation plays an important role in initiating and maintaining liver inflammation, and blockade of NKG2D recognition becomes a promising approach to alleviate liver inflammation. Treatment by silencing NKG2D ligands on hepatocytes, but not NKG2D on circulating immune cells, is more liver‐specific, and simultaneous knockdown of multiple NKG2D ligands on hepatocytes will be more efficient in liver disease intervention.