Critical role of tumor necrosis factor receptor 1, but not 2, in hepatic stellate cell proliferation, extracellular matrix remodeling, and liver fibrogenesis

Núria Tarrats, Anna Moles, Albert Morales, Carmen García‐Ruiz, José C. Fernández‐Checa, Montserrat Marí – 26 April 2011 – Tumor necrosis factor (TNF) has been implicated in the progression of many chronic liver diseases leading to fibrosis; however, the role of TNF in fibrogenesis is controversial and the specific contribution of TNF receptors to hepatic stellate cell (HSC) activation remains to be established.

The hepcidin circuits act: Balancing iron and inflammation

Bryan D. Maliken, James E. Nelson, Kris V. Kowdley – 22 April 2011 – Hepcidin is a peptide hormone that regulates iron homeostasis and acts as an antimicrobial peptide. It is expressed and secreted by a variety of cell types in response to iron loading and inflammation. Hepcidin mediates iron homeostasis by binding to the iron exporter ferroportin, inducing its internalization and degradation via activation of the protein kinase Jak2 and the subsequent phosphorylation of ferroportin.

Interleukin 2 receptor antagonists for liver transplant recipients: A systematic review and meta‐analysis of controlled studies

Armin D. Goralczyk, Nicola Hauke, Narin Bari, Tung Y. Tsui, Thomas Lorf, Aiman Obed – 21 April 2011 – Interleukin 2 receptor antagonists (IL‐2Ra) are frequently used as induction therapy in liver transplant recipients to decrease the risk of acute rejection while allowing the reduction of concomitant immunosuppression. We conducted a systematic review of prospective, controlled studies to test the hypothesis that the use of IL‐2Ra is associated with a decrease in acute rejection and/or a decrease in the side effects of concomitant medication.

Endpoints and clinical trial design for nonalcoholic steatohepatitis

Arun J. Sanyal, Elizabeth M. Brunt, David E. Kleiner, Kris V. Kowdley, Naga Chalasani, Joel E. Lavine, Vlad Ratziu, Arthur McCullough – 21 April 2011 – Nonalcoholic fatty liver disease is a common cause of chronic liver disease in the general population. Nonalcoholic steatohepatitis (NASH), the aggressive form of nonalcoholic fatty liver disease, is associated with an increased risk of liver‐related mortality and cardiovascular disease. At present, a liver biopsy is the only generally acceptable method for the diagnosis of NASH and assessment of its progression toward cirrhosis.

Mitochondria‐targeted ubiquinone (MitoQ) decreases ethanol‐dependent micro and macro hepatosteatosis

Balu K. Chacko, Anup Srivastava, Michelle S. Johnson, Gloria A. Benavides, Mi Jung Chang, Yaozu Ye, Nirag Jhala, Michael P. Murphy, Balaraman Kalyanaraman, Victor M. Darley‐Usmar – 21 April 2011 – Chronic alcohol‐induced liver disease results in inflammation, steatosis, and increased oxidative and nitrosative damage to the mitochondrion. We hypothesized that targeting an antioxidant to the mitochondria would prevent oxidative damage and attenuate the steatosis associated with alcoholic liver disease.

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