Myoblast models of skeletal muscle hypertrophy and atrophy

被引:33
|
作者
Sharples, Adam P. [1 ,2 ]
Stewart, Claire E. [2 ]
机构
[1] Univ Bedfordshire, Dept Sport & Exercise Sci, ISPAR Bedford,Fac Educ Sport & Tourism, Muscle Cellular & Mol Physiol Res Grp MCMP, Bedford MK41 9EA, England
[2] Manchester Metropolitan Univ, Fac Sci & Engn, Inst Biomed Res Human Movement & Hlth IRM, Manchester M15 6BH, Lancs, England
关键词
three-dimensional muscle constructs; insulin-like growth factor-I; muscle precursor cell; myostatin; satellite cell; MAJOR PHYSIOLOGICAL REGULATOR; BONE MORPHOGENETIC PROTEIN-2; GROWTH-FACTOR; POSTABSORPTIVE RATS; POSSIBLE MECHANISM; PHOSPHATIDIC-ACID; MYOSTATIN SIGNALS; COUNTERPOINT IGF; STEM-CELLS; DIFFERENTIATION;
D O I
10.1097/MCO.0b013e3283457ade
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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.
引用
收藏
页码:230 / 236
页数:7
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