Thioredoxin-1 attenuates sepsis-induced cardiomyopathy after cecal ligation and puncture in mice

Our results indicate that overexpression of Trx-1 attenuates cardiac dysfunction during CLP. The mechanism of action may involve reduction of oxidative stress, apoptosis, and vascular permeability through activation of Trx-1/HO-1 and anti-apoptotic protein survivin.