Overview
Skeletal muscle growth and adaptation require the contribution of a unique population of cells known as muscle stems (satellite cells). In response to damage or stress, muscle stem cells become activated, proliferate, and fuse with muscle fibers to repair damaged tissue. These cells are controlled by a series of transcriptional networks, collectively referred to as the myogenic regulatory factors that govern the induction of these cells from quiescence through proliferation and into terminal differentiation. What remains poorly understood is precisely what environmental cues, released in the hours and days following exercise-induced muscle damage, and how these cues interact with satellite cells? A related question, that is a focus of my laboratory, is what are the intracellular events that act downstream of these signals leading to the activation of the myogenic regulatory factors.
A second major focus of my laboratory involves revealing the mechanism(s) underlying the progressive loss of muscle mass associated with aging. It has been shown that muscle growth (hypertrophy) is not possible without the contribution of a functional muscle stem cell population. By extension, it stands to reason that a loss of muscle mass with aging, and a blunted hypertrophic response to chronic exercise in older adults, is likely a result of age-related muscle stem cell dysnfunction and/or age-related loss of muscle stem cell number. My research program aims to examine potential age-related impairment of muscle stem cells, as well as the molecular and cellular events that lead to dysregulation of muscle stem cells in advanced age.
