Myocyte-restricted HO-1 transgenic (TG) mice exhibited significantly increased post-infarction survival and decreased left ventricular dilatation, mechanical dysfunction, hypertrophy, interstitial fibrosis, and oxidative stress during chronic heart failure.[7] Although induction of HO-1 halts renal interstitial fibrosis, [8] the potential mechanisms remain unclear. This evidence concerns the gene HMOX1 and infarction.