
Abfrage | Programm/Institut/Gruppe | PSP-Element | Kontakt | Anhang | Verwendung | Publikation |
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Titel:
Mitochondrial thioredoxin reductase is essential for early postischemic myocardial protection |
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Apr 2012 | TOXI EH |
G-505200-001 |
Zischka |
PDF |
WB 2012-07-01 AR 2012-07-01 |
Publikation |
Core statement:
Myocardial infarction is the leading cause of death in most industrialized nations throughout the world. High levels of oxygen radicals (ROS) in response to infarction (ischemia/reperfusion) are a major trigger of cardiomyocyte cell death, although their mode of action is only beginning to be understood. Here, we show that targeted disruption of a key mitochondrial ROS-detoxifying enzyme sensitizes to myocardial ischemia/reperfusion injury through opening of the mitochondrial transition pore. Importantly, pharmacological intervention, either through inhibition of the mitochondrial pore or by regeneration of the ROS-sensitive cellular thiol-pool, allowed restoring myocardial function and preventing tissue damage. |
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