BCL2 and myocardial infarction: [2], [12], [22] In animal models, HO-1 in transgenic mice prevented angiotensin II-induced high reactive oxygen species and inflammatory cytokines in vascular smooth muscle, adjacent endothelial, and cardiomyocytes. [23] HO-1 over-expression by adenovirus-mediated transfection into rat hearts increased the anti-apoptotic Bcl-2 protein, decreased lipid peroxidation, proapoptotic Bax, and proinflammatory interleukin-1-beta protein levels in a myocardial infarction model [24].