Our laboratory studies several different aspects of skeletal muscle and cardiovascular physiology, principally focusing on changes in plasma membrane repair, cellular metabolism and calcium homeostasis in normal physiology and disease states. We are currently examining how aberrant store-operated calcium handling can contribute to the progression of muscular dystrophy and developing methods to block this calcium entry. Additionally, efforts in heart failure models will determine the mechanisms that contribute to uncoupling of intracellular calcium homeostasis in the failing cardiomyocytes. Further studies examine the role of tripartite motif (TRIM) family proteins in the membrane repair process. Membrane repair is a conserved cellular process where intracellular vesicles actively patch membrane disruptions to allow survival of the cell. While relevant in normal physiology, disruption of this process results in diseases, including muscular dystrophy, ischemic damage to the heart and neurodegeneration. Our group is examining the role of novel TRIM family proteins in regulating membrane repair and how these can be targeted as therapeutic interventions in a number of different diseases.