IDH2 deficiency promotes mitochondrial dysfunction and cardiac hypertrophy in mice
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Ku, Hyeong Jun | - |
dc.contributor.author | Ahn, Youngkeun | - |
dc.contributor.author | Lee, Jin Hyup | - |
dc.contributor.author | Park, Kwon Moo | - |
dc.contributor.author | Park, Jeen-Woo | - |
dc.date.accessioned | 2021-09-04T18:38:54Z | - |
dc.date.available | 2021-09-04T18:38:54Z | - |
dc.date.created | 2021-06-15 | - |
dc.date.issued | 2015-03 | - |
dc.identifier.issn | 0891-5849 | - |
dc.identifier.uri | https://scholar.korea.ac.kr/handle/2021.sw.korea/94253 | - |
dc.description.abstract | Cardiac hypertrophy, a risk factor for heart failure, is associated with enhanced oxidative stress in the mitochondria, resulting from high levels of reactive oxygen species (ROS). The balance between ROS generation and ROS detoxification dictates ROS levels. As such, disruption of these processes results in either increased or decreased levels of ROS. In previous publications, we have demonstrated that one of the primary functions of mitochondrial NADP(+)-dependent isocitrate dehydrogenase (IDH2) is to control the mitochondrial redox balance, and-thereby mediate the cellular defense against oxidative damage, via the production of NADPH. To explore the association between IDH2 expression and cardiac function, we measured myocardial hypertrophy, apoptosis, and contractile dysfunction in IDH2 knockout (idh2(-/-)) and wild-type (idh2(+/+)) mice. As expected, mitochondria from the hearts of knockout mice lacked IDH2 activity and the hearts of IDH2-deficient mice developed accelerated heart failure, increased levels of apoptosis and hypertrophy, and exhibited mitochondrial dysfunction, which was associated with a loss of redox homeostasis. Our results suggest that IDH2 plays an important role in maintaining both baseline mitochondrial function and cardiac contractile function following pressure-overload hypertrophy, by preventing oxidative stress. (C) 2014 Elsevier Inc. All rights reserved. | - |
dc.language | English | - |
dc.language.iso | en | - |
dc.publisher | ELSEVIER SCIENCE INC | - |
dc.subject | OXIDATIVE STRESS | - |
dc.subject | DEHYDROGENASE-ACTIVITY | - |
dc.subject | MYOCARDIAL-INFARCTION | - |
dc.subject | GLUTATHIONE | - |
dc.subject | HEART | - |
dc.subject | APOPTOSIS | - |
dc.subject | SUPEROXIDE | - |
dc.subject | ISCHEMIA | - |
dc.subject | DAMAGE | - |
dc.subject | RAT | - |
dc.title | IDH2 deficiency promotes mitochondrial dysfunction and cardiac hypertrophy in mice | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Lee, Jin Hyup | - |
dc.identifier.doi | 10.1016/j.freeradbiomed.2014.12.018 | - |
dc.identifier.scopusid | 2-s2.0-84921487385 | - |
dc.identifier.wosid | 000351485000009 | - |
dc.identifier.bibliographicCitation | FREE RADICAL BIOLOGY AND MEDICINE, v.80, pp.84 - 92 | - |
dc.relation.isPartOf | FREE RADICAL BIOLOGY AND MEDICINE | - |
dc.citation.title | FREE RADICAL BIOLOGY AND MEDICINE | - |
dc.citation.volume | 80 | - |
dc.citation.startPage | 84 | - |
dc.citation.endPage | 92 | - |
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.journalResearchArea | Endocrinology & Metabolism | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology | - |
dc.relation.journalWebOfScienceCategory | Endocrinology & Metabolism | - |
dc.subject.keywordPlus | OXIDATIVE STRESS | - |
dc.subject.keywordPlus | DEHYDROGENASE-ACTIVITY | - |
dc.subject.keywordPlus | MYOCARDIAL-INFARCTION | - |
dc.subject.keywordPlus | GLUTATHIONE | - |
dc.subject.keywordPlus | HEART | - |
dc.subject.keywordPlus | APOPTOSIS | - |
dc.subject.keywordPlus | SUPEROXIDE | - |
dc.subject.keywordPlus | ISCHEMIA | - |
dc.subject.keywordPlus | DAMAGE | - |
dc.subject.keywordPlus | RAT | - |
dc.subject.keywordAuthor | IDH2 | - |
dc.subject.keywordAuthor | Redox status | - |
dc.subject.keywordAuthor | Cardiac hypertrophy | - |
dc.subject.keywordAuthor | Apoptosis | - |
dc.subject.keywordAuthor | Mitochondria | - |
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.