Thioredoxin 2 protects mice against experimental myocardial infarction

Abstract

Experimental Myocardial infarction (MI) using ligation procedure induces cardiac dysfunction, high level of ROS, inflammation, apoptosis, fibrosis and cardiomyocyte (CM) loss. AAV overexpressing human Trx-2, specifically in CM mitochondria improves mouse cardiac function, reduces the size of cardiac infarct, increases the expression of cardiac anti-inflammatory markers, reduces apoptosis and oxidative stress. However, it does not increase CM proliferation.

Keywords

• myocardial infarction
• heart failure
• thioredoxin 2