Given that elevated expression of myocd is a frequent event in HF conditions [19], [21], [25], our results highlight the benefits of inhibiting the upregulated MYOCD signaling pathway in failing ventricular myocardium: a moderate myocd suppression was sufficient to downregulate the elevated expression of MYOCD-dependent SM-marker genes, ameliorate diastolic chamber dysfunction, and prevent pre-mature mortality of DHF animals. Here, MYOCD is linked to hydrops fetalis.