Mammals have limited cardiac regeneration capacity, after myocardial infarction. Recent studies have shown that newborn mice can fully regenerate myocardial cells after cryoinjury but loose this ability by the 7th day postnatally. In contrast, zebrafish retain their ability to regenerate their hearts throughout their lifetime. Studies in zebrafish already indicated cell types (epicardium) and a number of signaling pathways necessary for regeneration (Fgf). As a result the idea that re-activating or suppressing certain signaling pathways after myocardial infarction could result in stimulating the endogenous regenerating potential in mammals draws increasing interest. We use ventricular cryoinjury in zebrafish as a myocardial infarction model to study heart regeneration. We propose to do RNAseq analyses to identify signaling pathways that get activated or suppressed at different time points during zebrafish heart regeneration with the potential to test these pathways in mice and human cardiomyocytes.