Thioredoxin Attenuates Post-ischemic Damage in Ventricular and Mitochondrial Function

Abstract

Thioredoxin (Trx) is an important antioxidant cellular system that plays an important role in cardioprotection against ischemia/reperfusion injury. The cardioprotective effects include a reduction of infarct size and an amelioration of ventricular and mitochondrial dysfunction that occurs in myocardial stunning. Particularly, Trx1 plays a protective role against the oxidative stress caused by an increase of reactive oxygen species concentration, as occurs during the reperfusion after an ischemic episode, and also could activate proteins related to pro-survival pathways such as MAP-kinases, Akt and GSK3. It has been also shown that, at least partially, Trx-1 takes part of cardioprotective mechanisms such as ischemic preconditioning (PC) and postconditioning (PostC). However, comorbidities such as aging can modify this powerful cellular defense, leading to decrease cardioprotection, and even ischemic PC and PostC induced in aged animal models failed to decrease infarct size. Therefore, the lack of success of antioxidants therapies to treat ischemic heart disease could be solved avoiding the damage of Trx system.