Abstract
Recent advances in our understanding of the biology of muscle have led to new interest in the pharmacological treatment of muscle wasting. Loss of muscle mass and increased intramuscular fibrosis occur in both sarcopenia and muscular dystrophy. Several regulators (mammalian target of rapamycin, serum response factor, atrogin-1, myostatin, etc.) seem to modulate protein synthesis and degradation or transcription of muscle-specific genes during both sarcopenia and muscular dystrophy. This review provides an overview of the adaptive changes in several regulators of muscle mass in both sarcopenia and muscular dystrophy.
Highlights
In humans, skeletal muscle is the most abundant tissue in the body, comprising 40–50% of body mass and playing vital roles in locomotion, heat production during periods of cold stress, and overall metabolism
Endurance training leads to minor changes in skeletal muscle mass, strength training induces marked hypertrophy of exercising muscles
If we can understand more concretely and definitively the mechanisms underlying sarcopenia and muscular dystrophy, more effective applications for skeletal muscle wasting may be conducted in the near future
Summary
Reviewed by: Guo-Yuan Yang, Shanghai Jiao Tong University, China Fabio Demontis, St. Jude Children’s Research Hospital, USA. Recent advances in our understanding of the biology of muscle have led to new interest in the pharmacological treatment of muscle wasting. Loss of muscle mass and increased intramuscular fibrosis occur in both sarcopenia and muscular dystrophy. Several regulators (mammalian target of rapamycin, serum response factor, atrogin-1, myostatin, etc.) seem to modulate protein synthesis and degradation or transcription of muscle-specific genes during both sarcopenia and muscular dystrophy. This review provides an overview of the adaptive changes in several regulators of muscle mass in both sarcopenia and muscular dystrophy
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