Portosystemic collaterals in living donor liver transplantation: What is all the fuss about?

Mettu Srinivas Reddy, Mohamed Rela – 10 January 2017 – Portosystemic collaterals are a common finding in patients with cirrhosis undergoing liver transplantation. Recently, there has been a renewed interest regarding their significance in the setting of living donor liver transplantation (LDLT) due to concerns of graft hypoperfusion or hyperperfusion and its impact on early posttransplant outcomes.

CCBE1 mutation causing sclerosing cholangitis: Expanding the spectrum of lymphedema‐cholestasis syndrome

André Viveiros, Marion Reiterer, Benedikt Schaefer, Armin Finkenstedt, Stefan Schneeberger, Hubert Schwaighofer, Patrizia Moser, Rudolf Sprenger, Bernhard Glodny, Wolfgang Vogel, Andreas R. Janecke, Heinz Zoller – 10 January 2017 – A 52‐year old patient presented with lymphedema, protein loosing enteropathy, and sclerosing cholangitis and was diagnosed with lymphedema cholestasis syndrome (LCS).

A liver‐specific long noncoding RNA with a role in cell viability is elevated in human nonalcoholic steatohepatitis

Biljana Atanasovska, Sander S. Rensen, Marijke R. Sijde, Glenn Marsman, Vinod Kumar, Iris Jonkers, Sebo Withoff, Ronit Shiri‐Sverdlov, Jan Willem M. Greve, Klaas Nico Faber, Han Moshage, Cisca Wijmenga, Bart van de Sluis, Marten H. Hofker, Jingyuan Fu – 10 January 2017 – Hepatocyte apoptosis in nonalcoholic steatohepatitis (NASH) can lead to fibrosis and cirrhosis, which permanently damage the liver. Understanding the regulation of hepatocyte apoptosis is therefore important to identify therapeutic targets that may prevent the progression of NASH to fibrosis.

Activation of the c‐Jun N‐terminal kinase pathway aggravates proteotoxicity of hepatic mutant Z alpha1‐antitrypsin

Nunzia Pastore, Sergio Attanasio, Barbara Granese, Raffaele Castello, Jeffrey Teckman, Andrew A. Wilson, Andrea Ballabio, Nicola Brunetti‐Pierri – 10 January 2017 – Alpha1‐antitrypsin deficiency is a genetic disease that can affect both the lung and the liver. The vast majority of patients harbor a mutation in the serine protease inhibitor 1A (SERPINA1) gene leading to a single amino acid substitution that results in an unfolded protein that is prone to polymerization.

The PNPLA3 I148M variant modulates the fibrogenic phenotype of human hepatic stellate cells

Francesca Virginia Bruschi, Thierry Claudel, Matteo Tardelli, Alessandra Caligiuri, Thomas M. Stulnig, Fabio Marra, Michael Trauner – 10 January 2017 – The genetic polymorphism I148M of patatin‐like phospholipase domain–containing 3 (PNPLA3) is robustly associated with hepatic steatosis and its progression to steatohepatitis, fibrosis, and cancer. Hepatic stellate cells (HSCs) are key players in the development of liver fibrosis, but the role of PNPLA3 and its variant I148M in this process is poorly understood.

The PNPLA3 I148M variant modulates the fibrogenic phenotype of human hepatic stellate cells

Francesca Virginia Bruschi, Thierry Claudel, Matteo Tardelli, Alessandra Caligiuri, Thomas M. Stulnig, Fabio Marra, Michael Trauner – 10 January 2017 – The genetic polymorphism I148M of patatin‐like phospholipase domain–containing 3 (PNPLA3) is robustly associated with hepatic steatosis and its progression to steatohepatitis, fibrosis, and cancer. Hepatic stellate cells (HSCs) are key players in the development of liver fibrosis, but the role of PNPLA3 and its variant I148M in this process is poorly understood.

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