Molecular mechanisms of cardiac protection by adaptation to chronic hypoxia
Language English Country Czech Republic Media print
Document type Journal Article, Research Support, Non-U.S. Gov't, Review
PubMed
15119931
Knihovny.cz E-resources
- MeSH
- Potassium Channels physiology MeSH
- Adaptation, Physiological * MeSH
- Cell Hypoxia physiology MeSH
- Myocardial Ischemia prevention & control MeSH
- Humans MeSH
- Nitric Oxide physiology MeSH
- Protein Kinases physiology MeSH
- Reactive Oxygen Species MeSH
- Heart physiology MeSH
- Animals MeSH
- Check Tag
- Humans MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Review MeSH
- Names of Substances
- Potassium Channels MeSH
- Nitric Oxide MeSH
- Protein Kinases MeSH
- Reactive Oxygen Species MeSH
Effective protection of the heart against ischemia/reperfusion injury is one of the most important goals of experimental and clinical research in cardiology. Besides ischemic preconditioning as a powerful temporal protective phenomenon, adaptation to chronic hypoxia also increases cardiac tolerance to all major deleterious consequences of acute oxygen deprivation such as myocardial infarction, contractile dysfunction and ventricular arrhythmias. Although many factors have been proposed to play a potential role, the detailed mechanism of this long-term protection remains poorly understood. This review summarizes current limited evidence for the involvement of ATP-sensitive potassium channels, reactive oxygen species, nitric oxide and various protein kinases in cardioprotective effects of chronic hypoxia.
Sixty Years of Heart Research in the Institute of Physiology of the Czech Academy of Sciences
The involvement of protein kinases in the cardioprotective effect of chronic hypoxia
Selection of optimal reference genes for gene expression studies in chronically hypoxic rat heart
Up-regulation and redistribution of protein kinase C-δ in chronically hypoxic heart
Myocardial ischemic injury and protection
