We focus on myocardial remodeling due to insults to the heart such as hypertension or ischemia. The contribution of different cell types and the underlying molecular signaling is particularly interesting to us. Roughly half of the cells in the heart are myocytes, and other cell types such as fibroblasts, vascular cells, and leucocytes importantly contribute to the cardiac stress response. We employ in vivo models of ischemic and loading stress (aortic constriction, ischemia-reperfusion) that may be genetically modified. State-of-the art phenotyping of these models including imaging, telemetric surveillance, hemodynamic characterization using pressure-volume relationships are performed, and are complemented by immunohistochemistry/immunofluorescence and standard molecular biology techniques to dissect underlying signaling pathways. We also use human multicellular heart tissue to study cardiac function and assess calcium homeostasis in isolated single cardiomyocytes using confocal microscopy.