AMPK is critical for mitochondrial function during reperfusion after myocardial ischemia
DC Field | Value | Language |
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dc.contributor.author | Zaha, Vlad G. | - |
dc.contributor.author | Qi, Dake | - |
dc.contributor.author | Su, Kevin N. | - |
dc.contributor.author | Palmeri, Monica | - |
dc.contributor.author | Lee, Hui-Young | - |
dc.contributor.author | Hu, Xiaoyue | - |
dc.contributor.author | Wu, Xiaohong | - |
dc.contributor.author | Shulman, Gerald I. | - |
dc.contributor.author | Rabinovitch, Peter S. | - |
dc.contributor.author | Russell, Raymond R., III | - |
dc.contributor.author | Young, Lawrence H. | - |
dc.date.available | 2020-02-28T02:45:41Z | - |
dc.date.created | 2020-02-06 | - |
dc.date.issued | 2016-02 | - |
dc.identifier.issn | 0022-2828 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/8596 | - |
dc.description.abstract | AMP-activated kinase (AMPK) is a stress responsive kinase that regulates cellular metabolism and protects against cardiomyocyte injury during ischemia-reperfusion (IR). Mitochondria play an important role in cell survival, but the specific actions of activated AMPK in maintaining mitochondrial integrity and function during re perfusion are unknown. Thus, we assessed the consequences of AMPK inactivation on heart mitochondrial function during reperfusion. Mouse hearts expressing wild type (WT) or kinase-dead (KD) AMPK were studied. Mitochondria isolated from KD hearts during reperfusion had intact membrane integrity, but demonstrated reduced oxidative capacity, increased hydrogen peroxide production and decreased resistance to mitochondrial permeability transition pore opening compared to WT. KD hearts showed increased activation of the mitogen activated protein kinase kinase 4 (MKK4) and downstream c-Jun terminal kinase (JNK) and greater necrosis during reperfusion after coronary occlusion. Transgenic expression of mitochondrial catalase (MCAT) prevented the excessive cardiac JNK activation and attenuated the increased myocardial necrosis observed during reperfusion in KD mice. Inhibition of JNK increased the resistance of KD hearts to mPTP opening, contractile dysfunction and necrosis during IR. Thus, intrinsic activation of AMPK is critical to prevent excess mitochondriai reactive oxygen production and consequent JNK signaling during reperfusion, thereby protecting against mPTP opening, irreversible mitochondrial damage and myocardial injury. (C) 2015 Elsevier Ltd. All rights reserved. | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | ELSEVIER SCI LTD | - |
dc.relation.isPartOf | JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY | - |
dc.subject | ACTIVATED PROTEIN-KINASE | - |
dc.subject | PERMEABILITY TRANSITION PORE | - |
dc.subject | N-TERMINAL KINASE | - |
dc.subject | ENERGY-METABOLISM | - |
dc.subject | GLUCOSE-UPTAKE | - |
dc.subject | JNK PATHWAY | - |
dc.subject | CELL-DEATH | - |
dc.subject | HEART | - |
dc.subject | INJURY | - |
dc.subject | MUSCLE | - |
dc.title | AMPK is critical for mitochondrial function during reperfusion after myocardial ischemia | - |
dc.type | Article | - |
dc.type.rims | ART | - |
dc.description.journalClass | 1 | - |
dc.identifier.wosid | 000371370300015 | - |
dc.identifier.doi | 10.1016/j.yjmcc.2015.12.032 | - |
dc.identifier.bibliographicCitation | JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, v.91, pp.104 - 113 | - |
dc.identifier.scopusid | 2-s2.0-84953296173 | - |
dc.citation.endPage | 113 | - |
dc.citation.startPage | 104 | - |
dc.citation.title | JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY | - |
dc.citation.volume | 91 | - |
dc.contributor.affiliatedAuthor | Lee, Hui-Young | - |
dc.type.docType | Article | - |
dc.subject.keywordAuthor | Signal transduction | - |
dc.subject.keywordAuthor | Ischemia | - |
dc.subject.keywordAuthor | Reperfusion | - |
dc.subject.keywordAuthor | Mitochondria | - |
dc.subject.keywordAuthor | AMPK | - |
dc.subject.keywordPlus | ACTIVATED PROTEIN-KINASE | - |
dc.subject.keywordPlus | PERMEABILITY TRANSITION PORE | - |
dc.subject.keywordPlus | N-TERMINAL KINASE | - |
dc.subject.keywordPlus | ENERGY-METABOLISM | - |
dc.subject.keywordPlus | GLUCOSE-UPTAKE | - |
dc.subject.keywordPlus | JNK PATHWAY | - |
dc.subject.keywordPlus | CELL-DEATH | - |
dc.subject.keywordPlus | HEART | - |
dc.subject.keywordPlus | INJURY | - |
dc.subject.keywordPlus | MUSCLE | - |
dc.relation.journalResearchArea | Cardiovascular System & Cardiology | - |
dc.relation.journalResearchArea | Cell Biology | - |
dc.relation.journalWebOfScienceCategory | Cardiac & Cardiovascular Systems | - |
dc.relation.journalWebOfScienceCategory | Cell Biology | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
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