FTO and myocardial infarction: Conversely, overexpression of FTO in stressed hypoxic cardiomyocytes and failed mouse cardiomyocytes alleviates ischemia-induced cardiac remodeling, and loss of cardiac contractile-protein expression and cardiac contractile function; these events manifest as improvement in ejection fraction, short axis shortening rate, and ventricular wall motion in mice at 2 and 4 weeks after myocardial infarction.