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Uncouple my heart: the benefits of inefficiency
M. Modrianský, E. Gabrielová
Language English Country United States
Document type Review, Research Support, Non-U.S. Gov't
NLK
ProQuest Central
from 1997-02-01 to 1 year ago
Health & Medicine (ProQuest)
from 1997-02-01 to 1 year ago
- MeSH
- Cell Death drug effects MeSH
- Dinitrophenols therapeutic use MeSH
- Phenols therapeutic use MeSH
- Flavonoids therapeutic use MeSH
- Ion Channels metabolism MeSH
- Ischemic Preconditioning, Myocardial MeSH
- Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone therapeutic use MeSH
- Myocytes, Cardiac metabolism pathology MeSH
- Cardiotonic Agents therapeutic use MeSH
- Humans MeSH
- Mitochondrial Proteins metabolism MeSH
- Myocardium metabolism pathology MeSH
- Oxidative Phosphorylation MeSH
- Myocardial Reperfusion Injury drug therapy metabolism pathology MeSH
- Uncoupling Agents therapeutic use MeSH
- Signal Transduction drug effects MeSH
- Animals MeSH
- Check Tag
- Humans MeSH
- Animals MeSH
- Publication type
- Research Support, Non-U.S. Gov't MeSH
- Review MeSH
Myocardial ischemia/reperfusion (IR) injury leads to structural changes in the heart muscle later followed by functional decline due to progressive fibrous replacement. Hence approaches to minimize IR injury are devised, including ischemic pre-and postconditioning. Mild uncoupling of oxidative phosphorylation is one of the mechanisms suggested to be cardioprotective as chemical uncoupling mimics ischemic preconditioning. Uncoupling protein 2 is proposed to be the physiological counterpart of chemical uncouplers and is thought to be a part of the protective machinery of cardiomyocytes. Morphological changes in the mitochondrial network likely accompany the uncoupling with mitochondrial fission dampening the signals leading to cardiomyocyte death. Here we review recent data on the role of uncoupling in cardioprotection and propose that low concentrations of dietary polyphenols may elicit the same cardioprotective effect as dinitrophenol and FCCP, perhaps accounting for the famed "French paradox".
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- $a Myocardial ischemia/reperfusion (IR) injury leads to structural changes in the heart muscle later followed by functional decline due to progressive fibrous replacement. Hence approaches to minimize IR injury are devised, including ischemic pre-and postconditioning. Mild uncoupling of oxidative phosphorylation is one of the mechanisms suggested to be cardioprotective as chemical uncoupling mimics ischemic preconditioning. Uncoupling protein 2 is proposed to be the physiological counterpart of chemical uncouplers and is thought to be a part of the protective machinery of cardiomyocytes. Morphological changes in the mitochondrial network likely accompany the uncoupling with mitochondrial fission dampening the signals leading to cardiomyocyte death. Here we review recent data on the role of uncoupling in cardioprotection and propose that low concentrations of dietary polyphenols may elicit the same cardioprotective effect as dinitrophenol and FCCP, perhaps accounting for the famed "French paradox".
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