Rubicon inhibits autophagy and accelerates hepatocyte apoptosis and lipid accumulation in nonalcoholic fatty liver disease in mice

Satoshi Tanaka, Hayato Hikita, Tomohide Tatsumi, Ryotaro Sakamori, Yasutoshi Nozaki, Sadatsugu Sakane, Yuto Shiode, Tasuku Nakabori, Yoshinobu Saito, Naoki Hiramatsu, Keisuke Tabata, Tsuyoshi Kawabata, Maho Hamasaki, Hidetoshi Eguchi, Hiroaki Nagano, Tamotsu Yoshimori, Tetsuo Takehara – 16 September 2016 – Nonalcoholic fatty liver disease (NAFLD) is the most prevalent liver disease worldwide. It encompasses a spectrum ranging from simple steatosis to fatty liver with hepatocellular injury, termed nonalcoholic steatohepatitis.

Workforce in hepatology: Update and a critical need for more information

Mark W. Russo, Ayman A. Koteish, Michael Fuchs, K. Gautham Reddy, Oren K. Fix – 15 September 2016 – The field of hepatology has experienced dramatic changes since the last workforce study in hepatology over 15 years ago. Hepatology practice has been dominated by hepatitis C but is now being overtaken by patients with nonalcoholic fatty liver disease. Expertise once attainable only through informal training, hepatology now has an accredited fellowship pathway and is recognized as a distinct discipline from gastroenterology with its own board certification.

Hypoxia‐driven Hif2a coordinates mouse liver regeneration by coupling parenchymal growth to vascular expansion

Philipp Kron, Michael Linecker, Perparim Limani, Andrea Schlegel, Patryk Kambakamba, Jean‐Marie Lehn, Claude Nicolau, Rolf Graf, Bostjan Humar, Pierre‐Alain Clavien – 15 September 2016 – Interaction between sinusoidal endothelial cells and hepatocytes is a prerequisite for liver function. Upon tissue loss, both liver cell populations need to be regenerated. Repopulation occurs in a coordinated pattern, first through the regeneration of parenchyme (hepatocytes), which then produces vascular endothelial growth factor (VEGF) to enable the subsequent angiogenic phase.

IRAKM‐Mincle axis links cell death to inflammation: Pathophysiological implications for chronic alcoholic liver disease

Hao Zhou, Minjia Yu, Junjie Zhao, Bradley N. Martin, Sanjoy Roychowdhury, Megan R. McMullen, Emily Wang, Paul L. Fox, Sho Yamasaki, Laura E. Nagy, Xiaoxia Li – 15 September 2016 – Lipopolysaccharide (LPS)‐mediated activation of Toll‐like receptors (TLRs) in hepatic macrophages and injury to hepatocytes are major contributors to the pathogenesis of alcoholic liver disease. However, the mechanisms by which TLR‐dependent inflammatory responses and alcohol‐induced hepatocellular damage coordinately lead to alcoholic liver disease are not completely understood.

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