title: Myoblast models of skeletal muscle hypertrophy and atrophy.
abstract: OBJECTIVE
  To highlight recent breakthroughs and controversies in the use of myoblast models to uncover cellular and molecular mechanisms regulating skeletal muscle hypertrophy and atrophy.
  
  
  RESULTS
  Myoblast cultures provide key mechanistic models of the signalling and molecular pathways potentially employed by skeletal muscle in-vivo to regulate hypertrophy and atrophy. Recently the controversy as to whether insulin-like growth factor (IGF)-I is important in hypertrophy following mechanical stimuli vs. alternative pathways has been hotly debated and is discussed. The role of myostatin in myoblast models of atrophy and interactions between protein synthetic pathways including Akt/mTOR and the 'atrogenes' are explored.
  
  
  CONCLUSIONS
  Targeted in-vivo experimentation directed by skeletal muscle cell culture and bioengineering (three-dimensional skeletal muscle cell culture models) will provide key biomimetic and mechanistic data regarding hypertrophy and atrophy and thus enable the development of important strategies for tackling muscle wasting associated with ageing and disease processes.
authors: Muscle Cellular and Molecular Physiology Research Group (MCMP), Institute for Sport and Physical Activity Research Bedford, UK. adam.sharples@beds.ac.uk
authors: Adam P
authors: AP
authors: Sharples
authors: Claire E
authors: CE
authors: Stewart
mesh_terms: D006801:Humans; D006984:Hypertrophy / Q000378:metabolism; D007334:Insulin-Like Growth Factor I / Q000378:metabolism*; D008954:Models, Biological; D018482:Muscle, Skeletal / Q000254:growth & development / Q000473:pathology*; D009133:Muscular Atrophy / Q000378:metabolism*; D032448:Myoblasts, Skeletal / Q000502:physiology*; D055435:Myostatin / Q000378:metabolism*; D014176:Protein Biosynthesis / Q000502:physiology*; D015398:Signal Transduction; D013314:Stress, Mechanical
chemical_list: D055435:Myostatin; D007334:Insulin-Like Growth Factor I