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GPx7 ameliorates non-alcoholic steatohepatitis by regulating oxidative stress

DC Field Value Language
dc.contributor.author황성순-
dc.contributor.author김재우-
dc.date.accessioned2020-09-29T00:47:20Z-
dc.date.available2020-09-29T00:47:20Z-
dc.date.issued2020-06-
dc.identifier.issn1976-6696-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/179396-
dc.description.abstractNon-alcoholic fatty liver disease (NAFLD) is one of the most common liver diseases. NAFLD can further progress to irreversible liver failure such as non-alcoholic steatohepatitis (NASH) fibrosis and cirrhosis. However, specific regulator of NASH fibrosis has yet to be established. Here, we found that glutathione peroxidase 7 (GPx7) was markedly expressed in NASH fibrosis. Although GPx7 is an antioxidant enzyme protecting other organs, whether GPx7 plays a role in NASH fibrosis has yet to be studied. We found that knockdown of GPx7 in transforming growth factor-β (TGF-β) and free fatty acids (FFA)-treated LX-2 cells elevated the 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 the expression of pro-fibrotic and pro-inflammatory genes. Further, NASH fibrosis induced by choline-deficient amino acid defined, high fat diet (CDAHFD) feeding was significantly accelerated by knockdown of GPx7, as evidenced by up-regulated liver fibrosis and inflammation compared with CDAHFD control mice. Collectively, these results suggest that GPx7 might be a novel therapeutic target to prevent the progression and development of NAFLD.-
dc.description.statementOfResponsibilityopen-
dc.languageEnglish-
dc.publisherKorean Society for Biochemistry and Molecular Biology-
dc.relation.isPartOfBMB REPORTS-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.titleGPx7 ameliorates non-alcoholic steatohepatitis by regulating oxidative stress-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentBioMedical Science Institute (의생명과학부)-
dc.contributor.googleauthorHyeon Ju Kim-
dc.contributor.googleauthorYoseob Lee-
dc.contributor.googleauthorSungsoon Fang-
dc.contributor.googleauthorWon Kim-
dc.contributor.googleauthorHyo Jung Kim-
dc.contributor.googleauthorJae-Woo Kim-
dc.identifier.doi10.5483/BMBRep.2020.53.6.280-
dc.contributor.localIdA05443-
dc.contributor.localIdA00865-
dc.relation.journalcodeJ00348-
dc.identifier.eissn1976-670X-
dc.identifier.pmid32317079-
dc.contributor.alternativeNameFang, Sungsoon-
dc.contributor.affiliatedAuthor황성순-
dc.contributor.affiliatedAuthor김재우-
dc.citation.volume53-
dc.citation.number6-
dc.citation.startPage317-
dc.citation.endPage322-
dc.identifier.bibliographicCitationBMB REPORTS, Vol.53(6) : 317-322, 2020-06-
Appears in Collections:
1. College of Medicine (의과대학) > BioMedical Science Institute (의생명과학부) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Biochemistry and Molecular Biology (생화학-분자생물학교실) > 1. Journal Papers

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