Abstract
The loss of muscle stem cell (MuSC) numbers and function in the elderly results in a dramatic delay or incomplete repair of muscle following injury or surgery. Prolonged immobility can exacerbate the loss of muscle mass with increased morbidity of affected patients. Stem cells and their niche cooperate to regulate the activation, self-renewal, differentiation, and return to quiescence of MuSCs. Extracellular matrix fibronectin (FN) and MuSC β1-integrin have been identified as critical factors in the dysfunction of aging muscle. Reduced amounts and/or function of β1-integrin and fibronectin are critical factors in the decline in MuSC regeneration and homeostasis with aging. Replacement of fibronectin and/or stimulation of β1-integrin may provide a novel means to augment the decline in MuSC function with age.
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