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Mitochondrial thioredoxin reductase is essential for early postischemic myocardial protection

Apr 2012 TOXI
Zischka PDF WB 2012-07-01
AR 2012-07-01
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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