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This galley proof is being listed electronically before publishing the final manuscript (It's not final version).

GPx7 ameliorates non-alcoholic steatohepatitis by regulating oxidative stress
Hyeon Ju Kim1,2, Yoseob Lee1,2, Sungsoon Fang2,3, Won Kim4, Hyo Jung Kim1,#, Jae-woo Kim1,2,*,#
1Dept. Biochemistry and Molecular Biology, Yonsei University College of Medicine,
2Brain Korea 21 PLUS Project for Medical Science, Yonsei University,
3Severance Biomedical Science Institute, Yonsei University College of Medicine,
4Department of Internal Medicine, Seoul National University College of Medicine
Non-alcoholic fatty liver disease (NAFLD) is one of the most common liver disease. NAFLD can progress to further irreversible liver failure such as non-alcoholic steatohepatitis (NASH)-fibrosis and cirrhosis. However, specific regulator of NASH-fibrosis has not been established yet. Here, we found that glutathione peroxidase 7 (GPx7) was markedly expressed in NASH-fibrosis. Although GPx7 is known as antioxidant enzyme to protect other organs, whether GPx7 plays a role in NASH-fibrosis has not been studied yet. We found that knockdown of GPx7 in transforming growth factor-モ (TGF-モ) and free fatty acids (FFA)-treated LX-2 cells elevated expression of pro-fibrotic and pro-inflammatory genes and collagen synthesis. Consistently, GPx7 overexpression in LX-2 cells led to the suppression of ROS production and reduced expression of pro-fibrotic and pro-inflammatory genes. Moreover, choline-deficient amino acid defined, high fat diet (CDAHFD) feeding-induced NASH-fibrosis was significantly accelerated by knockdown of GPx7, as evidenced by up-regulated liver fibrosis and inflammation compared to CDAHFD control mice. Collectively, these results suggest that GPx7 might be a novel therapeutic target to prevent the progression and development of NAFLD.
Abstract, Accepted Manuscript(in press) [Submitted on November 11, 2019, Accepted on December 2, 2019]
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