The biological function of insulin-like growth factor-I in myogenesis and its therapeutic effect on muscular dystrophy.
In progressive muscular dystrophy, such as Duchenne muscular dystrophy, muscles show the pathological changes characterized by hypertrophy at the early phase, while atrophic changes are seen with aging. As an experimental model for muscle hypertrophy and atrophy, insulin-like growth factor-1 (IGF-1) signaling via the activation of PI3K/Akt pathway has been well characterized. IGF-1 is also highlighted as a therapeutic agent as it has been shown to improve phenotype of dystrophic animals. In this review, the functions of IGF-1 on mitogenic proliferation and myogenic differentiation in vitro, muscle hypertrophy in vivo are discussed, as well as its possible utility for molecular therapy on muscular dystrophies.
Noguchi
S
S
Department of Neuromuscular Research, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Tokyo, Japan. noguchi@ncnp.go.jp
D000818:Animals; D002454:Cell Differentiation / Q000502:physiology; D002470:Cell Survival / Q000502:physiology; D006801:Humans; D006984:Hypertrophy; D007334:Insulin-Like Growth Factor I / Q000502:physiology*; D020929:Mitogen-Activated Protein Kinase Kinases / Q000502:physiology; D032342:Muscle Cells / Q000473:pathology; D018482:Muscle, Skeletal / Q000378:metabolism; D009136:Muscular Dystrophies / Q000473:pathology / Q000503:physiopathology*; D009137:Muscular Dystrophy, Animal / Q000503:physiopathology; D020388:Muscular Dystrophy, Duchenne / Q000473:pathology / Q000503:physiopathology; D019869:Phosphatidylinositol 3-Kinases / Q000502:physiology; D015398:Signal Transduction / Q000502:physiology; D015854:Up-Regulation / Q000502:physiology
D007334:Insulin-Like Growth Factor I; D019869:Phosphatidylinositol 3-Kinases; D020929:Mitogen-Activated Protein Kinase Kinases