Alcoholic liver disease

Alcoholic liver disease is liver damage that results from alcohol misuse. The least severe stage of alcoholic liver disease is alcoholic fatty liver disease, followed by alcoholic hepatitis and then alcoholic cirrhosis; some overlap exists between these stages. Symptoms generally occur only once the liver has been severely damaged.

Latest Research and Reviews

  • Research |

    In patients with alcoholic hepatitis, cytolysin-positive Enterococcus faecalis strains are correlated with liver disease severity and increased mortality, and in mouse models these strains can be specifically targeted by bacteriophages.

    • Yi Duan
    • , Cristina Llorente
    • , Sonja Lang
    • , Katharina Brandl
    • , Huikuan Chu
    • , Lu Jiang
    • , Richard C. White
    • , Thomas H. Clarke
    • , Kevin Nguyen
    • , Manolito Torralba
    • , Yan Shao
    • , Jinyuan Liu
    • , Adriana Hernandez-Morales
    • , Lauren Lessor
    • , Imran R. Rahman
    • , Yukiko Miyamoto
    • , Melissa Ly
    • , Bei Gao
    • , Weizhong Sun
    • , Roman Kiesel
    • , Felix Hutmacher
    • , Suhan Lee
    • , Meritxell Ventura-Cots
    • , Francisco Bosques-Padilla
    • , Elizabeth C. Verna
    • , Juan G. Abraldes
    • , Robert S. Brown Jr
    • , Victor Vargas
    • , Jose Altamirano
    • , Juan Caballería
    • , Debbie L. Shawcross
    • , Samuel B. Ho
    • , Alexandre Louvet
    • , Michael R. Lucey
    • , Philippe Mathurin
    • , Guadalupe Garcia-Tsao
    • , Ramon Bataller
    • , Xin M. Tu
    • , Lars Eckmann
    • , Wilfred A. van der Donk
    • , Ry Young
    • , Trevor D. Lawley
    • , Peter Stärkel
    • , David Pride
    • , Derrick E. Fouts
    •  & Bernd Schnabl
    Nature 575, 505-511
  • Research
    | Open Access

    Alcoholic hepatitis, a common cause of liver failure, lacks effective treatment. Here, the authors show altered hepatic HNF4a isoform expression and hypermethylation of its target genes in patients. HNF4a dysregulation is improved in vitro by TGFb or PPARg modulation suggesting potential therapeutic avenues.

    • Josepmaria Argemi
    • , Maria U. Latasa
    • , Stephen R. Atkinson
    • , Ilya O. Blokhin
    • , Veronica Massey
    • , Joel P. Gue
    • , Joaquin Cabezas
    • , Juan J. Lozano
    • , Derek Van Booven
    • , Aaron Bell
    • , Sheng Cao
    • , Lawrence A. Vernetti
    • , Juan P. Arab
    • , Meritxell Ventura-Cots
    • , Lia R. Edmunds
    • , Constantino Fondevilla
    • , Peter Stärkel
    • , Laurent Dubuquoy
    • , Alexandre Louvet
    • , Gemma Odena
    • , Juan L. Gomez
    • , Tomas Aragon
    • , Jose Altamirano
    • , Juan Caballeria
    • , Michael J. Jurczak
    • , D. Lansing Taylor
    • , Carmen Berasain
    • , Claes Wahlestedt
    • , Satdarshan P. Monga
    • , Marsha Y. Morgan
    • , Pau Sancho-Bru
    • , Philippe Mathurin
    • , Shinji Furuya
    • , Carolin Lackner
    • , Ivan Rusyn
    • , Vijay H. Shah
    • , Mark R. Thursz
    • , Jelena Mann
    • , Matias A. Avila
    •  & Ramon Bataller
  • Research
    | Open Access

    Dysregulation of PPARα dependent fatty acid oxidation promotes hepatic steatosis. Here the authors show that GPS2 inhibits PPARα activity and that ablation of GPS2 ameliorates hepatic steatosis in mice.

    • Ning Liang
    • , Anastasius Damdimopoulos
    • , Saioa Goñi
    • , Zhiqiang Huang
    • , Lise-Lotte Vedin
    • , Tomas Jakobsson
    • , Marco Giudici
    • , Osman Ahmed
    • , Matteo Pedrelli
    • , Serena Barilla
    • , Fawaz Alzaid
    • , Arturo Mendoza
    • , Tarja Schröder
    • , Raoul Kuiper
    • , Paolo Parini
    • , Anthony Hollenberg
    • , Philippe Lefebvre
    • , Sven Francque
    • , Luc Van Gaal
    • , Bart Staels
    • , Nicolas Venteclef
    • , Eckardt Treuter
    •  & Rongrong Fan

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