Our research focuses on the regulation of myogenic stem cell function in adult life. Our long-term goal is to identify means to ameliorate age-related muscle
deterioration (sarcopenia) and combat muscle wasting in muscular dystrophy. Sarcopenia is characterized by a decline in mass, strength, and endurance of skeletal muscles, and by fat
accumulation between and within myofibers. Subtle muscle injuries that occur during routine muscle activity raise a continuous demand for functional myofiber repair throughout life.
However, myogenic stem cell performance declines in old age and this decline can be a contributory factor to sarcopenia. We investigate satellite cells, classically defined tissue
specific myogenic stem cells that reside beneath the myofiber basal lamina, as well as non-myogenic progenitors associated with the microvasculature that may contribute to myogenesis by
myogenic reprogramming. Our research approach is based on the view that muscle aging is not an isolated event that starts late in life, but rather a continuum of ongoing developmental
biology processes that progress with life.
The following research areas are pursued:
Mechanisms involved in supporting myogenic
commitment and renewal of satellite cells. The role of FGF-FGFR system in regulating satellite cells. The role of Klotho genes in the balance between myogenicity and adiposity
of skeletal muscle.
Origin and cellular/molecular distinctions of
satellite cells from extraocular muscles (EOM) that contribute to enhanced stem cell performance and sparing from muscular dystrophy.
Origin and significance of
unconventional progenitors that may function to replace myonuclei during myofiber maintenance. Emphasis is given to the role of cells associated with the microvasculature, in
particular the pericytes.
Current funding: National Institutes of Health (NIA, NIAMS), Muscular Dystrophy Association.