Regulation of skeletal muscle size, function, and adaptation.

My current research program is centered on the study of the neuromuscular system and its response and adaptation to various stressors, including aging. Skeletal muscle is a particularly interesting tissue because it interacts with and responds to numerous systems and signals to control movement, as well as, glucose homeostasis, metabolism, and thermogenesis. The recent focus of my research has been on identifying the cellular and molecular mechanisms that regulate skeletal muscle mass, especially under atrophy inducing conditions. Skeletal muscle loss occurs as the result of a variety of disparate conditions including: disuse, bed rest, spinal cord injury, neurodegeneration, diabetes, cancer, chronic glucocorticoid treatment and aging; and will affect every individual in their lifetime as the result of aging. My laboratory is interested in identifying the mechanisms responsible for muscle atrophy and determining strategies for preventing atrophy or accelerating recovery following a period of muscle loss. In the quest to understand muscle atrophy, we have also investigated the mechanisms that regulate adaptive muscle growth, or hypertrophy, in adult animals. My laboratory was instrumental in the identification of two muscle specific E3 Ubiquitin Ligases: MuRF1 and MAFbx, in skeletal muscle, and we continue to examine the role of these two ligases in the regulation of skeletal muscle growth and atrophy, with recent emphasis on identifying the specific substrates regulated by MuRF1 and MAFbx. Finally, my lab is pursuing research to identify the molecular mediators of the health benefits of exercise.



Department/Program Affiliations:
Internal Medicine