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Updated: Jun 3, 2026

Modeling Myotonic Dystrophy 1 in C2C12 Myoblast Cells
Published on: July 29, 2016
Myoblast models of skeletal muscle hypertrophy and atrophy
Adam P Sharples1, Claire E Stewart
1Muscle Cellular and Molecular Physiology Research Group (MCMP), Institute for Sport and Physical Activity Research Bedford, UK. adam.sharples@beds.ac.uk
Purpose Of Review:
To highlight recent breakthroughs and controversies in the use of myoblast models to uncover cellular and molecular mechanisms regulating skeletal muscle hypertrophy and atrophy.
Recent Findings:
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.
Summary:
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.
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