Open AccessObeticholic acid attenuates human immunodeficiency virus/alcohol metabolism-induced pro-fibrotic activation in liver cells
Author(s) -
Moses New-Aaron,
Murali Ganesan,
Raghubendra Singh Dagur,
Kusum K. Kharbanda,
Larisa Y. Poluektova,
Natalia A. Osna
Publication year - 2020
Publication title -
world journal of hepatology
Language(s) - Uncategorized
Resource type - Journals
SCImago Journal Rank - 0.913
H-Index - 55
ISSN - 1948-5182
DOI - 10.4254/wjh.v12.i11.965
Subject(s) - medicine , liver injury , cyp2e1 , timp1 , apoptosis , inflammasome , alcoholic liver disease , western blot , hepatocyte , immunology , liver disease , cancer research , virology , biology , cirrhosis , inflammation , metabolism , gene expression , biochemistry , cytochrome p450 , in vitro , gene
The morbidity and mortality of human immunodeficiency virus (HIV)-infection is often associated with liver disease, which progresses slowly into severe liver dysfunction. There are multiple insults which exacerbate HIV-related liver injury, including HIV-associated dysregulation of lipid metabolism and fat turnover, co-infections with hepatotropic viruses and alcohol abuse. As we reported before, exposure of hepatocytes to HIV and alcohol metabolites causes high oxidative stress, impairs proteasomal and lysosomal functions leading to accumulation of HIV in these cells, which end-ups with apoptotic cell death and finally promotes development of liver fibrosis.