In view of the robust ventricular remodeling observed after myocardial infarction, the role of oxidative stress–mediated reduction in myocardial angiogenesis and the antioxidative and growth regulatory action of Grx-1, we have hypothesized that overexpression of Grx-1 in the myocardium would be beneficial in promoting neovascularization and preventing subsequent ventricular remodeling after myocardial infarction through upregulation of pro-angiogenic and anti-apoptotic molecules. The gene discussed is GLRX; the disease is myocardial infarction.