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MBOAT7 rs641738 increases risk of liver inflammation and transition to fibrosis in chronic hepatitis C

Author

Listed:
  • Khaled Thabet

    (Storr Liver Centre, Westmead Institute for Medical Research and Westmead Hospital, University of Sydney
    Faculty of Pharmacy, Minia University)

  • Anastasia Asimakopoulos

    (Storr Liver Centre, Westmead Institute for Medical Research and Westmead Hospital, University of Sydney)

  • Maryam Shojaei

    (Centre for Immunology and Allergy Research, Westmead Institute for Medical Research
    Nepean Genomic Research Group, ICU, Nepean Hospital)

  • Manuel Romero-Gomez

    (Unit for The Clinical Management of Digestive Diseases and CIBERehd, Hospital Universitario de Valme)

  • Alessandra Mangia

    (Ospedale Casa Sollievo della Sofferenza, IRCCS)

  • William L. Irving

    (NIHR Biomedical Research Unit in Gastroenterology and the Liver, University of Nottingham)

  • Thomas Berg

    (Section of Hepatology, Clinic for Gastroenterology and Rheumatology, University Clinic Leipzig)

  • Gregory J. Dore

    (Kirby Institute, The University of New South Wales)

  • Henning Grønbæk

    (Aarhus University Hospital)

  • David Sheridan

    (Institute of Translational and Stratified Medicine, Plymouth University)

  • Maria Lorena Abate

    (University of Turin)

  • Elisabetta Bugianesi

    (University of Turin)

  • Martin Weltman

    (Nepean Hospital)

  • Lindsay Mollison

    (Fremantle Hospital)

  • Wendy Cheng

    (Royal Perth Hospital)

  • Stephen Riordan

    (Gastrointestinal and Liver Unit, Prince of Wales Hospital and University of New South Wales)

  • Janett Fischer

    (Section of Hepatology, Clinic for Gastroenterology and Rheumatology, University Clinic Leipzig)

  • Ulrich Spengler

    (University of Bonn)

  • Jacob Nattermann

    (University of Bonn)

  • Ahmed Wahid

    (Faculty of Pharmacy, Minia University)

  • Angela Rojas

    (Unit for The Clinical Management of Digestive Diseases and CIBERehd, Hospital Universitario de Valme)

  • Rose White

    (Storr Liver Centre, Westmead Institute for Medical Research and Westmead Hospital, University of Sydney)

  • Mark W. Douglas

    (Storr Liver Centre, Westmead Institute for Medical Research and Westmead Hospital, University of Sydney
    Centre for Infectious Diseases and Microbiology, Marie Bashir Institute for Infectious Diseases and Biosecurity, University of Sydney at Westmead Hospital)

  • Duncan McLeod

    (Institute of Clinical Pathology and Medical Research (ICPMR), Westmead Hospital)

  • Elizabeth Powell

    (Princess Alexandra Hospital, School of Medicine, The University of Queensland)

  • Christopher Liddle

    (Storr Liver Centre, Westmead Institute for Medical Research and Westmead Hospital, University of Sydney)

  • David van der Poorten

    (Storr Liver Centre, Westmead Institute for Medical Research and Westmead Hospital, University of Sydney)

  • Jacob George

    (Storr Liver Centre, Westmead Institute for Medical Research and Westmead Hospital, University of Sydney)

  • Mohammed Eslam

    (Storr Liver Centre, Westmead Institute for Medical Research and Westmead Hospital, University of Sydney)

Abstract

Cirrhosis likely shares common pathophysiological pathways despite arising from a variety of liver diseases. A recent GWAS identified rs641738, a polymorphism in the MBOAT7 locus, as being associated with the development of alcoholic cirrhosis. Here we explore the role of this variant on liver inflammation and fibrosis in two cohorts of patients with chronic hepatitis C. In 2,051 patients, rs641738 associated with severe hepatic inflammation and increased risk of fibrosis, as well as fast fibrosis progression. At functional level, rs641738 associated with MBOAT7 transcript and protein levels in liver and blood, and with serum inflammatory, oxidative stress and macrophage activation markers. MBOAT7 was expressed in immune cell subsets, implying a role in hepatic inflammation. We conclude that the MBOAT7 rs641738 polymorphism is a novel risk variant for liver inflammation in hepatitis C, and thereby for liver fibrosis.

Suggested Citation

  • Khaled Thabet & Anastasia Asimakopoulos & Maryam Shojaei & Manuel Romero-Gomez & Alessandra Mangia & William L. Irving & Thomas Berg & Gregory J. Dore & Henning Grønbæk & David Sheridan & Maria Lorena, 2016. "MBOAT7 rs641738 increases risk of liver inflammation and transition to fibrosis in chronic hepatitis C," Nature Communications, Nature, vol. 7(1), pages 1-8, November.
    • Handle: RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms12757
    DOI: 10.1038/ncomms12757
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    Cited by:

    1. Jawaher Alharthi & Ali Bayoumi & Khaled Thabet & Ziyan Pan & Brian S. Gloss & Olivier Latchoumanin & Mischa Lundberg & Natalie A. Twine & Duncan McLeod & Shafi Alenizi & Leon A. Adams & Martin Weltman, 2022. "A metabolic associated fatty liver disease risk variant in MBOAT7 regulates toll like receptor induced outcomes," Nature Communications, Nature, vol. 13(1), pages 1-19, December.

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