MAJOR RESEARCH INTERESTS
Mechanisms of human skeletal muscle regeneration and muscle mass regulation are the major emphases in our laboratory. Muscle atrophy and reduced functional capacity are well-established, deleterious consequences of acute (e.g., surgery, trauma, disuse, burn) and chronic (e.g., Parkinson’s disease, arthritis, cancer, heart failure, spinal cord injury) conditions—the most widespread and insidious of which is the degenerative process of normal aging. Our research priorities span three, inter-related focus areas: (i) to determine the cellular and molecular mechanisms driving muscle regeneration following damage, surgery, or injury, while identifying differences responsible for regeneration impairment in certain phenotypes; (ii) to determine key processes responsible for myofiber hypertrophy, and to exploit these processes with countermeasures to promote muscle re-growth in conditions that induce muscle atrophy; and (iii) to better understand the primary etiology of muscle atrophy in acute and chronic conditions. We have a keen interest in the role of proinflammatory cytokine signaling on skeletal muscle atrophy, regrowth, and regeneration, and recently identified a state of muscle inflammation susceptibility (MuIS) in humans involving TWEAK and TNF-α/NFĸB signaling that is noted in vivo and inhibits satellite (stem) cell behavior in vitro. We suspect MuIS is a key determinant of individual responsiveness to treatments promoting muscle re-growth including exercise training.
