Charles DeRossi, Kathryn Bambino, Joshua Morrison, Isabel Sakarin, Carlos Villacorta‐Martin, Changwen Zhang, Jillian L. Ellis, M. Isabel Fiel, Maria Ybanez, Youngmin A. Lee, Kuan‐lin Huang, Chunyue Yin, Takuya F. Sakaguchi, Scott L. Friedman, Augusto Villanueva, Jaime Chu – 23 April 2019 – The growing burden of liver fibrosis and lack of effective antifibrotic therapies highlight the need for identification of pathways and complementary model systems of hepatic fibrosis.

Alexandre Balaphas, Jeremy Meyer, Karin Sadoul, Pierre Fontana, Philippe Morel, Carmen Gonelle‐Gispert, Leo H. Bühler – 22 April 2019 – Beyond their role in hemostasis, platelets are proposed as key mediators of several physiological and pathophysiological processes of the liver, such as liver regeneration, toxic or viral acute liver injury, liver fibrosis, and carcinogenesis. The effects of platelets on the liver involve interactions with sinusoidal endothelial cells and the release of platelet‐contained molecules following platelet activation.

Adrien Guillot, Frank Tacke – 22 April 2019 – Inflammation is a hallmark of virtually all liver diseases, such as liver cancer, fibrosis, nonalcoholic steatohepatitis, alcoholic liver disease, and cholangiopathies. Liver macrophages have been thoroughly studied in human disease and mouse models, unravelling that the hepatic mononuclear phagocyte system is more versatile and complex than previously believed. Liver macrophages mainly consist of liver‐resident phagocytes, or Kupffer cells (KCs), and bone marrow‐derived recruited monocytes.

Jordi Gracia‐Sancho, Nicolò Manicardi, Martí Ortega‐Ribera, Raquel Maeso‐Díaz, Sergi Guixé‐Muntet, Anabel Fernández‐Iglesias, Diana Hide, Héctor García‐Calderó, Zoe Boyer‐Díaz, Patricia C. Contreras, Alfred Spada, Jaime Bosch – 22 April 2019 – In cirrhosis, liver microvascular dysfunction is a key factor increasing hepatic vascular resistance to portal blood flow, which leads to portal hypertension. De‐regulated inflammatory and pro‐apoptotic processes due to chronic injury play important roles in the dysfunction of liver sinusoidal cells.

Hiroyoshi Doi, Sachiyo Yoshio, Keiichiro Yoneyama, Hironari Kawai, Yuzuru Sakamoto, Tomonari Shimagaki, Yoshihiko Aoki, Yosuke Osawa, Hitoshi Yoshida, Tatsuya Kanto – 22 April 2019 – Global implementation of a birth‐dose hepatitis B (HB) vaccine has significantly reduced the prevalence of hepatitis B virus (HBV) carriers. Durable and sufficient titers of antibodies to hepatitis B surface antigen (anti‐HBs) are desirable for vaccinees to gain resistance to HBV exposure.

Kenneth Cusi – 21 April 2019

Matthew J. Stotts, Opaku Adjapong, David E. Kaplan – 20 April 2019

Qing Li, Xiongxiong Pan, Deming Zhu, Zhengming Deng, Runqiu Jiang, Xuehao Wang – 20 April 2019 – Glucose metabolism reprogramming, which is a well‐established characteristic of multiple cancers, demands a higher rate of glycolysis to meet the increasing demands for macromolecular synthesis and to maintain rapid proliferation in a hypoxic environment. However, the mechanism underlying this switch remains to be elucidated. In this study, we investigated the function of circular RNA MAT2B (circMAT2B) in hepatocellular carcinoma (HCC) glucose metabolism reprogramming and malignancy.

Yan Xie, Hitoshi Matsumoto, Susan Kennedy, Elizabeth P. Newberry, William Moritz, Brian J. DeBosch, Kelle H. Moley, Deborah C. Rubin, Brad W. Warner, Andrew L. Kau, Phillip I. Tarr, Todd N. Wylie, Kristine M. Wylie, Nicholas O. Davidson – 20 April 2019 – The mechanisms by which alterations in intestinal bile acid (BA) metabolism improve systemic glucose tolerance and hepatic metabolic homeostasis are incompletely understood.

Yuanguo Wang, Kangsheng Tu, Donglian Liu, Luyang Guo, Yunru Chen, Qing Li, Jessica L. Maiers, Zhikui Liu, Vijay H. Shah, Changwei Dou, Daniel Tschumperlin, Luke Voneschen, Rendong Yang, Ningling Kang – 20 April 2019 – Nuclear translocation of mothers against decapentaplegic homolog 2/3 (SMAD2/3), core transcription factors of transforming growth factor β (TGF‐β) signaling, is critical for hepatic stellate cell (HSC) differentiation into metastasis‐promoting myofibroblasts.