Nonalcoholic fatty liver disease impairs expression of the type II inositol 1,4,5‐trisphosphate receptor

Tanaporn Khamphaya, Natsasi Chukijrungroat, Vitoon Saengsirisuwan, Kisha A. Mitchell‐Richards, Marie E. Robert, Albert Mennone, Meenakshisundaram Ananthanarayanan, Michael H. Nathanson, Jittima Weerachayaphorn – 10 October 2017 – Nonalcoholic fatty liver disease (NAFLD) is the most prevalent liver disease worldwide. It may result in several types of liver problems, including impaired liver regeneration (LR), but the mechanism for this is unknown.

Dual catenin loss in murine liver causes tight junctional deregulation and progressive intrahepatic cholestasis

Tirthadipa Pradhan‐Sundd, Lili Zhou, Ravi Vats, An Jiang, Laura Molina, Sucha Singh, Minakshi Poddar, Jacquelyn Russell, Donna B Stolz, Michael Oertel, Udayan Apte, Simon Watkins, Sarangarajan Ranganathan, Kari N. Nejak‐Bowen, Prithu Sundd, Satdarshan Pal Monga – 10 October 2017 – β‐Catenin, the downstream effector of the Wnt signaling, plays important roles in hepatic development, regeneration, and tumorigenesis. However, its role at hepatocyte adherens junctions (AJ) is relatively poorly understood, chiefly due to spontaneous compensation by γ‐catenin.

MicroRNA 15a/16‐1 suppresses aryl hydrocarbon receptor–dependent interleukin‐22 secretion in CD4+ T cells and contributes to immune‐mediated organ injury

Zhou Lu, Jiajing Liu, Xiaoming Liu, Enyu Huang, Jiao Yang, Jiawen Qian, Dan Zhang, Ronghua Liu, Yiwei Chu – 10 October 2017 – Interleukin‐22 (IL‐22), as a link between leukocytic and nonleukocytic cells, has gained increasing attention for its pronounced tissue‐protective properties. MicroRNAs, emerging as crucial immune modulators, have been reported to be involved in the production and action of various cytokines. However, the precise control of IL‐22 by microRNAs and its subsequent actions remained to be elucidated.

Polycystic liver disease: Hepatic venous outflow obstruction lesions of the noncystic parenchyma have major consequences

Louise Barbier, Maxime Ronot, Béatrice Aussilhou, François Cauchy, Claire Francoz, Valérie Vilgrain, Olivier Soubrane, Valérie Paradis, Jacques Belghiti – 10 October 2017 – In patients with polycystic liver disease (PLD), development of cysts induces hepatic venous outflow obstruction (HVOO) and parenchymal modifications, challenging the paradigm of a normal noncystic liver parenchyma.

Placental growth factor inhibition targets pulmonary angiogenesis and represents a therapy for hepatopulmonary syndrome in mice

Sarah Raevens, Anja Geerts, Annelies Paridaens, Sander Lefere, Xavier Verhelst, Anne Hoorens, Jo Van Dorpe, Tania Maes, Ken R. Bracke, Christophe Casteleyn, Bart Jonckx, Thomas Horvatits, Valentin Fuhrmann, Hans Van Vlierberghe, Christophe Van Steenkiste, Lindsey Devisscher, Isabelle Colle – 10 October 2017 – Hepatopulmonary syndrome (HPS) is a severe complication of cirrhosis with increased risk of mortality. Pulmonary microvascular alterations are key features of HPS; but underlying mechanisms are incompletely understood, and studies on HPS are limited to rats.

Cholangiocyte autophagy contributes to hepatic cystogenesis in polycystic liver disease and represents a potential therapeutic target

Anatoliy I. Masyuk, Tatyana V. Masyuk, Maria J. Lorenzo Pisarello, Jingyi (Francess) Ding, Lorena Loarca, Bing Q. Huang, Nicholas F. LaRusso – 10 October 2017 – Polycystic liver disease (PLD) is a group of genetic disorders with limited treatment options and significant morbidity. Hepatic cysts arise from cholangiocytes exhibiting a hyperproliferative phenotype.

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