A chronic increase in reactive oxygen species (ROS) plays a critical role in the development and progression of cardiac remodeling associated with heart failure. Oxidative stress is indeed increased in heart failure, hypertension, cardiac fibrosis and hypertrophy. In vitro exposure of cardiac fibroblasts to superoxide anion stimulates their proliferation by increasing the production of transforming growth factor-β1 (TGF-β1), a potent fibrogenic cytokine. TGF-β1 plays an important role in cardiac development, cardiac hypertrophy, ventricular remodeling and the early response to myocardial infarction. In this review the role of TGF-β1 and ROS in the production and deposition of collagens by cardiac fibroblasts and in the induction of gene expression in relation to the development of myocardial fibrosis and to myocardial tissue repair will be discussed.