Striated muscle (skeletal and cardiac muscle) undergoes remodeling, either positive or negative, in response to physiological and pathological stress. For example, many inflammatory diseases including cancer, AIDS, sepsis, diabetes, and congestive heart failure induce debilitating muscle atrophy or wasting due to loss of muscle mass (cachexia). On the other hand, diseased or injured muscle has the capacity to regenerate leading to recovery of muscle mass and function. In addition, cardiac muscle chronically exposed to high blood pressure develops hypertrophy and eventually left ventricle dilation (congestive heart failure). The research in my lab is aimed to dissect the signaling mechanisms that regulate the remodeling processes using cellular and molecular approaches, and to test therapeutic strategies using in vitro and in vivo models. We are currently working on three research projects.