Amelioration of late-onset hepatic steatosis in IDH2-deficient mice
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Lee, Su Jeong | - |
dc.contributor.author | Cha, Hanvit | - |
dc.contributor.author | Kim, Hyunjin | - |
dc.contributor.author | Lee, Jin Hyup | - |
dc.contributor.author | Park, Jeen-Woo | - |
dc.date.accessioned | 2021-09-03T14:59:21Z | - |
dc.date.available | 2021-09-03T14:59:21Z | - |
dc.date.created | 2021-06-16 | - |
dc.date.issued | 2017 | - |
dc.identifier.issn | 1071-5762 | - |
dc.identifier.uri | https://scholar.korea.ac.kr/handle/2021.sw.korea/86307 | - |
dc.description.abstract | Nonalcoholic fatty liver disease (NAFLD) has a high prevalence in the general population and can evolve into nonalcoholic steatohepatosis (NASH), cirrhosis, and complications such as liver failure and hepatocellular carcinoma. Recently, we reported that mitochondrial NADP(+)-dependent isocitrate dehydrogenase, encoded by the IDH2, plays an important role in the regulation of redox balance and oxidative stress levels, which are tightly associated with intermediary metabolism and energy production. In the present study, we showed that in mice targeted disruption of IDH2 attenuates age-associated hepatic steatosis by the activation of p38/cJun NH2-terminal kinase (JNK) and p53, presumably induced by the elevation of mitochondrial reactive oxygen species (ROS), which in turn resulted in the suppression of hepatic lipogenesis and inflammation via the upregulation of fibroblast growth factor 21 (FGF21) and the inhibition of NFB signaling pathways. Our finding uncovers a new mechanism involved in hepatocellular steatosis and IDH2 may be a valuable therapeutic target for the management of NAFLD. | - |
dc.language | English | - |
dc.language.iso | en | - |
dc.publisher | TAYLOR & FRANCIS LTD | - |
dc.subject | FATTY LIVER-DISEASE | - |
dc.subject | ACETYL-COA CARBOXYLASE | - |
dc.subject | GROWTH-FACTOR 21 | - |
dc.subject | NF-KAPPA-B | - |
dc.subject | INSULIN-RESISTANCE | - |
dc.subject | BINDING-PROTEIN | - |
dc.subject | MITOCHONDRIAL DYSFUNCTION | - |
dc.subject | ISOCITRATE DEHYDROGENASE | - |
dc.subject | IKK-BETA | - |
dc.subject | ACTIVATION | - |
dc.title | Amelioration of late-onset hepatic steatosis in IDH2-deficient mice | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Lee, Jin Hyup | - |
dc.identifier.doi | 10.1080/10715762.2017.1320554 | - |
dc.identifier.scopusid | 2-s2.0-85018263400 | - |
dc.identifier.wosid | 000401520100004 | - |
dc.identifier.bibliographicCitation | FREE RADICAL RESEARCH, v.51, no.4, pp.368 - 374 | - |
dc.relation.isPartOf | FREE RADICAL RESEARCH | - |
dc.citation.title | FREE RADICAL RESEARCH | - |
dc.citation.volume | 51 | - |
dc.citation.number | 4 | - |
dc.citation.startPage | 368 | - |
dc.citation.endPage | 374 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology | - |
dc.subject.keywordPlus | FATTY LIVER-DISEASE | - |
dc.subject.keywordPlus | ACETYL-COA CARBOXYLASE | - |
dc.subject.keywordPlus | GROWTH-FACTOR 21 | - |
dc.subject.keywordPlus | NF-KAPPA-B | - |
dc.subject.keywordPlus | INSULIN-RESISTANCE | - |
dc.subject.keywordPlus | BINDING-PROTEIN | - |
dc.subject.keywordPlus | MITOCHONDRIAL DYSFUNCTION | - |
dc.subject.keywordPlus | ISOCITRATE DEHYDROGENASE | - |
dc.subject.keywordPlus | IKK-BETA | - |
dc.subject.keywordPlus | ACTIVATION | - |
dc.subject.keywordAuthor | IDH2 | - |
dc.subject.keywordAuthor | hepatosteatosis | - |
dc.subject.keywordAuthor | mitochondrial ROS | - |
dc.subject.keywordAuthor | FGF21 | - |
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.
145 Anam-ro, Seongbuk-gu, Seoul, 02841, Korea+82-2-3290-2963
COPYRIGHT © 2021 Korea University. All Rights Reserved.
Certain data included herein are derived from the © Web of Science of Clarivate Analytics. All rights reserved.
You may not copy or re-distribute this material in whole or in part without the prior written consent of Clarivate Analytics.