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Title: MBOAT7 rs641738 increases risk of liver inflammation and transition to fibrosis in chronic hepatitis C.
Authors: Thabet, Khaled
Asimakopoulos, Anastasia
Shojaei, Maryam
Romero-Gomez, Manuel
Mangia, Alessandra
Irving, William L
Berg, Thomas
Dore, Gregory J
Grønbæk, Henning
Sheridan, David
Abate, Maria Lorena
Bugianesi, Elisabetta
Weltman, Martin
Mollison, Lindsay
Cheng, Wendy
Riordan, Stephen
Fischer, Janett
Spengler, Ulrich
Nattermann, Jacob
Wahid, Ahmed
Rojas, Angela
White, Rose
Douglas, Mark W
McLeod, Duncan
Powell, Elizabeth
Liddle, Christopher
van der Poorten, David
George, Jacob
Eslam, Mohammed
International Liver Disease Genetics Consortium
metadata.dc.subject.mesh: Acyltransferases
Carcinoma, Hepatocellular
Case-Control Studies
Cohort Studies
Disease Progression
Fatty Liver
Hepatitis C, Chronic
Immune System
Liver Cirrhosis
Liver Neoplasms
Macrophage Activation
Membrane Proteins
Middle Aged
Oxidative Stress
Polymorphism, Single Nucleotide
Issue Date: 15-Sep-2016
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.
metadata.dc.identifier.doi: 10.1038/ncomms12757
Appears in Collections:Producción 2020

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