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A new \u2018chemogenetic\u2019 animal model of heart failure reproduces a critical characteristic shared by many disease states that lead to heart failure in humans: <jats:italic>an increase in redox stress in the heart.<\/jats:italic> This \u2018chemogenetic\u2019 approach exploits a recombinant yeast enzyme that can be dynamically and specifically activated in vivo to generate the ROS hydrogen peroxide (H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub>) in cardiac myocytes. Redox stress can be rapidly, selectively and reversibly manipulated by chemogenetic generation of ROS in cardiac myocytes, yielding a new model of dilated cardiomyopathy. Treatment of animals with the angiotensin receptor antagonist valsartan promotes recovery of ventricular function and resolution of adverse cardiac remodelling. 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