Role of satellite cells in muscle growth and maintenance of muscle mass. Nutr Metab Cardiovasc Dis [Epub ahead of print]

Department of Biomedical Sciences, University of Padova, Padova, Italy.
Nutrition, metabolism, and cardiovascular diseases: NMCD (Impact Factor: 3.32). 05/2012; 23. DOI: 10.1016/j.numecd.2012.02.002
Source: PubMed


Changes in muscle mass may result from changes in protein turnover, reflecting the balance between protein synthesis and protein degradation, and changes in cell turnover, reflecting the balance between myonuclear accretion and myonuclear loss. Myonuclear accretion, i.e. increase in the number of myonuclei within the muscle fibers, takes place via proliferation and fusion of satellite cells, myogenic stem cells associated to skeletal muscle fibers and involved in muscle regeneration. In developing muscle, satellite cells undergo extensive proliferation and most of them fuse with myofibers, thus contributing to the increase in myonuclei during early postnatal stages. A similar process is induced in adult skeletal muscle by functional overload and exercise. In contrast, satellite cells and myonuclei may undergo apoptosis during muscle atrophy, although it is debated whether myonuclear loss occurs in atrophying muscle. An increase in myofiber size can also occur by changes in protein turnover without satellite cell activation, e.g. in late phases of postnatal development or in some models of muscle hypertrophy. The relative role of protein turnover and cell turnover in muscle adaptation and in the establishment of functional muscle hypertrophy remains to be established. The identification of the signaling pathways mediating satellite cell activation may provide therapeutic targets for combating muscle wasting in a variety of pathological conditions, including cancer cachexia, renal and cardiac failure, neuromuscular diseases, as well as aging sarcopenia.

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    • "Muscle growth involves a tightly controlled balance between protein synthesis and degradation [1]. Protein synthesis is driven by the growth hormone (GH)/Insulin like growth factor (IGF)/mammalian target of rapamycin (mTOR) pathway [2-5], whereas protein degradation occurs via a number of pathways including ubiquitin proteasome [6-8], lysosomal [9], apoptotic [10] and the calcium dependant calpains [11]. "
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    • "Analysis of the contractility of single fibers from MSTN null mice demonstrated that the specific force deficits were at the level of the muscle myofiber [80,81▪▪]. Historically, it has been thought that a major function of myostatin was to maintain muscle satellite cell quiescence and that the relief of this inhibitory influence led to satellite proliferation and fusion to existing myofibers resulting in hypertrophy, akin to the mechanisms of muscle enlargement after exercise [81▪▪,82]. However, recent evidence demonstrates that myostatin exerts its effects directly on the myofiber with little effect on satellite cell activity [83▪]. "
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    ABSTRACT: This review summarizes recent progress in the development of myostatin inhibitors for the treatment of muscle wasting disorders. It also focuses on findings in myostatin biology that may have implications for the development of antimyostatin therapies. There has been progress in evaluating antimyostatin therapies in animal models of muscle wasting disorders. Some programs have progressed into clinical development with initial results showing positive impact on muscle volume.In normal mice myostatin deficiency results in enlarged muscles with increased total force but decreased specific force (total force/total mass). An increase in myofibrillar protein synthesis without concomitant satellite cell proliferation and fusion leads to muscle hypertrophy with unchanged myonuclear number. A specific force reduction is not observed when atrophied muscle, the predominant therapeutic target of myostatin inhibitor therapy, is made myostatindeficient.Myostatin has been shown to be expressed by a number of tumor cell lines in mice and man. Myostatin inhibition remains a promising therapeutic strategy for a range of muscle wasting disorders.This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivitives 3.0 License, where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially.
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    • "Satellite cells in muscle disease therapy and future perspectives Sarcopenia, the loss of muscle fibers at an advanced age, is one of the major causes for falls and subsequently health deterioration in the elderly. The underlying reason for the reduced muscle mass is not entirely clear, and the contribution of age-related changes in satellite stem cell is under debate (Pallafacchina et al. 2012; Shadrach and Wagers 2011). Most other muscle diseases including the muscular dystrophies are genetic disorders associated with progressive muscle weakness and degeneration. "
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