Mixed lineage kinase 3 mediates release of C‐X‐C motif ligand 10–bearing chemotactic extracellular vesicles from lipotoxic hepatocytes

Samar H. Ibrahim, Petra Hirsova, Kyoko Tomita, Steven F. Bronk, Nathan W. Werneburg, Stephen A. Harrison, Val S. Goodfellow, Harmeet Malhi, Gregory J. Gores – 25 September 2015 – Mixed lineage kinase 3 (MLK3) deficiency reduces macrophage‐associated inflammation in a murine model of nonalcoholic steatohepatitis (NASH). However, the mechanistic links between MLK3 activation in hepatocytes and macrophage‐driven inflammation in NASH are uncharted.

Interferon lambda 4 genotypes and resistance‐associated variants in patients infected with hepatitis C virus genotypes 1 and 3

Kai‐Henrik Peiffer, Lisa Sommer, Simone Susser, Johannes Vermehren, Eva Herrmann, Matthias Döring, Julia Dietz, Dany Perner, Caterina Berkowski, Stefan Zeuzem, Christoph Sarrazin – 25 September 2015 – Single‐nucleotide polymorphisms (SNPs) in the interferon lambda 4 (IFNL4) gene are predictors for treatment success in patients with hepatitis C virus (HCV) infection. For direct‐acting antiviral combinations only weak association with IFNL4 SNPs was observed. Little is known about potential selections of resistance‐associated variants (RAVs) by the IFNL4 genotype.

Vasopressin 1a receptor partial agonism increases sodium excretion and reduces portal hypertension and ascites in cirrhotic rats

Guillermo Fernández‐Varo, Denise Oró, Edward Earl Cable, Vedrana Reichenbach, Silvia Carvajal, Bernardino González de la Presa, Kazimierz Wiśniewski, Pere Ginés, Geoffrey Harris, Wladimiro Jiménez – 24 September 2015 – Patients and rats with cirrhosis and ascites have portal hypertension and circulatory dysfunction. Synthetic arginine vasopressin (AVP) receptor agonists able to induce systemic and mesenteric vasoconstriction have shown their usefulness in reducing portal pressure (PP) in this condition.

Eliciting the mitochondrial unfolded protein response by nicotinamide adenine dinucleotide repletion reverses fatty liver disease in mice

Karim Gariani, Keir J. Menzies, Dongryeol Ryu, Casey J. Wegner, Xu Wang, Eduardo R. Ropelle, Norman Moullan, Hongbo Zhang, Alessia Perino, Vera Lemos, Bohkyung Kim, Young‐Ki Park, Alessandra Piersigilli, Tho X. Pham, Yue Yang, Chai Siah Ku, Sung I. Koo, Anna Fomitchova, Carlos Cantó, Kristina Schoonjans, Anthony A.

Eliciting the mitochondrial unfolded protein response by nicotinamide adenine dinucleotide repletion reverses fatty liver disease in mice

Karim Gariani, Keir J. Menzies, Dongryeol Ryu, Casey J. Wegner, Xu Wang, Eduardo R. Ropelle, Norman Moullan, Hongbo Zhang, Alessia Perino, Vera Lemos, Bohkyung Kim, Young‐Ki Park, Alessandra Piersigilli, Tho X. Pham, Yue Yang, Chai Siah Ku, Sung I. Koo, Anna Fomitchova, Carlos Cantó, Kristina Schoonjans, Anthony A.

Activation of the p62‐Keap1‐NRF2 pathway protects against ferroptosis in hepatocellular carcinoma cells

Xiaofang Sun, Zhanhui Ou, Ruochan Chen, Xiaohua Niu, De Chen, Rui Kang, Daolin Tang – 24 September 2015 – Ferroptosis is a recently recognized form of regulated cell death caused by an iron‐dependent accumulation of lipid reactive oxygen species. However, the molecular mechanisms regulating ferroptosis remain obscure. Here, we report that nuclear factor erythroid 2‐related factor 2 (NRF2) plays a central role in protecting hepatocellular carcinoma (HCC) cells against ferroptosis.

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