Key result
Thioredoxin-1 overexpression confers resistance to myocardial ischemia-reperfusion injury in mice.
Thioredoxins are a class of small redox-regulating proteins that appear to play a crucial role in many oxidative stress-inducible degenerative diseases. A recent study demonstrated a reduction of thioredoxin-1 (Trx1) protein in the ischemic reperfused myocardium. When the same heart was adapted to ischemic stress by preconditioning with repeated cyclic episodes of small duration of ischemia and reperfusion, there was an increased induction of Trx1 expression. Inhibition of Trx1 expression resulted in reduced postischemic ventricular recovery and increased myocardial infarct size in the preconditioned heart. Corroborating these findings, transgenic mouse hearts overexpressing Trx1 were resistant to ischemic reperfusion injury as compared with the hearts from wild-type mice. Thus, it appears that thioredoxin plays a crucial role in cardioprotection induced by preconditioning.
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Dipak K. Das (2004) studied Ischemic reperfusion injury. Thioredoxin-1 (Trx1) overexpression vs. Wild-type mice was evaluated on Ischemic reperfusion injury (myocardial infarct size and postischemic ventricular recovery). Thioredoxin-1 overexpression in transgenic mouse hearts conferred resistance to ischemic reperfusion injury compared with wild-type mice.
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