RT Journal Article
T1 MBOAT7 rs641738 increases risk of liver inflammation and transition to fibrosis in chronic hepatitis C.
A1 Thabet, Khaled
A1 Asimakopoulos, Anastasia
A1 Shojaei, Maryam
A1 Romero-Gomez, Manuel
A1 Mangia, Alessandra
A1 Irving, William L
A1 Berg, Thomas
A1 Dore, Gregory J
A1 Grønbæk, Henning
A1 Sheridan, David
A1 Abate, Maria Lorena
A1 Bugianesi, Elisabetta
A1 Weltman, Martin
A1 Mollison, Lindsay
A1 Cheng, Wendy
A1 Riordan, Stephen
A1 Fischer, Janett
A1 Spengler, Ulrich
A1 Nattermann, Jacob
A1 Wahid, Ahmed
A1 Rojas, Angela
A1 White, Rose
A1 Douglas, Mark W
A1 McLeod, Duncan
A1 Powell, Elizabeth
A1 Liddle, Christopher
A1 van der Poorten, David
A1 George, Jacob
A1 Eslam, Mohammed
A1 International Liver Disease Genetics Consortium, 
AB 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.
YR 2016
FD 2016-09-15
LK http://hdl.handle.net/10668/10446
UL http://hdl.handle.net/10668/10446
LA en
DS RISalud
RD Apr 7, 2025