Molecular mechanisms of cardiac protection by adaptation to chronic hypoxia
Jazyk angličtina Země Česko Médium print
Typ dokumentu časopisecké články, práce podpořená grantem, přehledy
PubMed
15119931
Knihovny.cz E-zdroje
- MeSH
- draslíkové kanály fyziologie MeSH
- fyziologická adaptace * MeSH
- hypoxie buňky fyziologie MeSH
- ischemická choroba srdeční prevence a kontrola MeSH
- lidé MeSH
- oxid dusnatý fyziologie MeSH
- proteinkinasy fyziologie MeSH
- reaktivní formy kyslíku MeSH
- srdce fyziologie MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- přehledy MeSH
- Názvy látek
- draslíkové kanály MeSH
- oxid dusnatý MeSH
- proteinkinasy MeSH
- reaktivní formy kyslíku 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
