Molecular mechanisms involving IGF-1 and myostatin to induce muscle hypertrophy as a therapeutic strategy for Duchenne muscular dystrophy.
Over the past decade, signalling cascades have been characterised that control key features of muscle growth, including the proliferation, differentiation of muscle precursors, the control cell size (hypertrophy) and cell death. In this review we highlight how two differing signalling molecules, Insulin-like Growth Factor-1 (IGF-1) and myostatin, regulate key steps during muscle development. We discuss how IGF-1 and myostatin signalling cascades can be manipulated to stimulate muscle growth. We summarise experimental data from mdx mouse, the animal model for Duchenne muscular dystrophy, that suggest a therapeutic value of these strategies for patients suffering from muscular dystrophy without redressing the primary cause of the lesion.
Patel
K
K
Veterinary Basic Sciences, Royal Veterinary College, Royal College Street, London England, UK. kpatel@rvc.ac.uk
Macharia
R
R
Amthor
H
H
D000818:Animals; D006801:Humans; D007334:Insulin-Like Growth Factor I / Q000502:physiology*; D051379:Mice; D018101:Mice, Inbred mdx; D024510:Muscle Development / Q000502:physiology*; D009122:Muscle Hypertonia / Q000209:etiology*; D020388:Muscular Dystrophy, Duchenne / Q000503:physiopathology / Q000628:therapy*; D055435:Myostatin; D015398:Signal Transduction / Q000502:physiology*; D016212:Transforming Growth Factor beta / Q000502:physiology*
C525911:MSTN protein, human; C525912:Mstn protein, mouse; D055435:Myostatin; D016212:Transforming Growth Factor beta; D007334:Insulin-Like Growth Factor I