Theterogeneous patterns of ventricular function in the 2 models, both exhibit increased intracellular calcium influx that is unaffected by metoprolol. Thus, overall responses to The tubs were placed at a common shelf height in a completely randomized design at the JARTU laborator metoprolol in both models are largely either absent or potentially detrimental. In clinical heart failure, right ventricular dysfunction is an important predictor of outcomes. In muscular dystrophy cardiomyopathy, right ventricular dysfunction may be an important early feature. In Becker��s muscular dystrophy cardiac involvement appears to develop first in the right ventricle when seen in younger patients, and left ventricular involvement develops at a later age. In the mdx mouse model, right ventricular dysfunction has also been shown to be an important early feature, and similarly to the clinical studies above, right ventricular dysfunction precedes left ventricular dysfunction. This suggests that the pathophysiology of right ventricular dysfunction is due to an intrinsic right ventricular process as opposed to right ventricular dysfunction developing secondary to left ventricular dysfunction in the setting of secondary pulmonary hypertension and increased right ventricular afterload. The detrimental effect of metroprolol on this early marker of cardiomyopathy in the mdx mice would suggest caution for early beta-blocker usage. One potential explanation linking the apparent improvement in left ventricular function and deterioration in right ventricular function is that the relatively low stroke volume from the left ventricle without treatment protects the abnormal and susceptible right ventricle from excessive volume overload. However, the betablockers restore stroke volume and cardiac output to wild type levels and this increased flow to the right side of the heart then causes greater dilatation of the right ventricle. This is a phenomenon that is well recognized when patients with biventricular dysfunction have left ventricular output restored with a left ventricular assist device that then aggravates right ventricular dysfunction. Increased calcium influx into the cardiac myocyte is an important phenomenon in muscular dystrophy cardiomyopathy leading to progression of left ventricular dysfunction. Recurrent membrane injury leads to an increased influx of calcium which then causes downstream effects such as activation of calcium-dependent hypertrophic pathways, reactive oxygen species and cell death through necrosis with mitochondrial defects. MEMRI can be used to non-invasively assess myocardial calcium influx, and we have recently shown that it is increased in these 2 mouse models. Despite the similar increase in calcium influx in both models we showed that there were likely different mechanisms responsible for this in the 2 models. Treatment with the beta-blocker metoprolol at an early stage in the development of the cardiomyopathy leads to worsening right ventricular function in the mdx mouse, and in both models has no effect on calcium influx. This suggests that clinical studies with beta-blockers and other heart failure medications should comprehensively evaluate not only left ventricular function but also right ventricular function and other aspect of myocardial metabolism. Protein-protein interactions are important for many fundamental cellular processes, and high-throughput proteomics studies have shown that most proteins interact with other proteins. The experimental elucidation of the of protein-protein complexes structures, however, is laborious and not always successful.