Pathological cardiac hypertrophy occurs as a consequence of adaptive responses to pressure or volume overload, mutations in sarcomeric (or other) proteins, or loss of contractile mass from prior infarction. While initially compensatory, over time when the heart can no longer meet with the increased metabolic demands of the mechanical work load imposed on the heart, dilation and heart failure ensue. Several signaling pathways are critically important in mediating myocardial hypertrophy, including the G-protein coupled receptor, the calcineurin/NFAT, MAPK, and the PI3K/ AKT/mTOR signaling pathways. Importantly, these signaling pathways also control molecular processes, such as cell proliferation, differentiation, survival, migration and other functions of the cell. In addition, the heart is comprised of several cell lineages make up the heart, including cardiomyocytes, fi broblasts, endothelial cells, and vascular smooth muscle cells, each integrally involved in modulating the signaling events that promote the