TY - JOUR
T1 - Cellular mechanisms and local progenitor activation to regulate skeletal muscle mass
AU - Cassano, Marco
AU - Quattrocelli, Mattia
AU - Crippa, Stefania
AU - Perini, Ilaria
AU - Ronzoni, Flavio
AU - Sampaolesi, Maurilio
N1 - Funding Information:
Acknowledgment Our work is supported by grants from FWO Odysseus Program n. G.0907.08; Wicka Funds n. zkb8720; the Italian Ministry of University and Scientific Research (grant n. 2005067555_003, PRIN 2006–08), Association Francoise contre les Myopathies, FP7 CARE-MI n.242038 and CARIPLO Foundation (grants n. 2007.5639 2008.2005). We are grateful to Catherine Ver-faillie, Giulio Cossu and Danny Huleybrook for continuous support and Gianpaolo Papaccio for helpful discussion. We thank, Christina Vochten and Luigi Vercesi for the professional secretarial service, and Paolo Luban for a kind donation. We apologize to colleagues whose work could not be cited due to space limitations.
PY - 2009/12
Y1 - 2009/12
N2 - Skeletal muscle hypertrophy is a result of increased load, such as functional and stretch-overload. Activation of satellite cells and proliferation, differentiation and fusion are required for hypertrophy of overloaded skeletal muscles. On the contrary, a dramatic loss of skeletal muscle mass determines atrophy settings. The epigenetic changes involved in gene regulation at DNA and chromatin level are critical for the opposing phenomena, muscle growth and atrophy. Physiological properties of skeletal muscle tissue play a fundamental role in health and disease since it is the most abundant tissue in mammals. In fact, protein synthesis and degradation are finely modulated to maintain an appropriate muscle mass. When the molecular signaling is altered muscle wasting and weakness occurred, and this happened in most common inherited and acquired disorders such as muscular dystrophies, cachexia, and age-related wasting. To date, there is no accepted treatment to improve muscle size and strength, and these conditions pose a considerable anxiety to patients as well as to public health. Several molecules, including Magic-F1, myostatin inhibitor, IGF, glucocorticoids and microRNAs are currently investigated to interfere positively in the blueprint of skeletal muscle growth and regeneration.
AB - Skeletal muscle hypertrophy is a result of increased load, such as functional and stretch-overload. Activation of satellite cells and proliferation, differentiation and fusion are required for hypertrophy of overloaded skeletal muscles. On the contrary, a dramatic loss of skeletal muscle mass determines atrophy settings. The epigenetic changes involved in gene regulation at DNA and chromatin level are critical for the opposing phenomena, muscle growth and atrophy. Physiological properties of skeletal muscle tissue play a fundamental role in health and disease since it is the most abundant tissue in mammals. In fact, protein synthesis and degradation are finely modulated to maintain an appropriate muscle mass. When the molecular signaling is altered muscle wasting and weakness occurred, and this happened in most common inherited and acquired disorders such as muscular dystrophies, cachexia, and age-related wasting. To date, there is no accepted treatment to improve muscle size and strength, and these conditions pose a considerable anxiety to patients as well as to public health. Several molecules, including Magic-F1, myostatin inhibitor, IGF, glucocorticoids and microRNAs are currently investigated to interfere positively in the blueprint of skeletal muscle growth and regeneration.
KW - AKT
KW - Magic-F1
KW - Muscle hypertrophy
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U2 - 10.1007/s10974-010-9204-y
DO - 10.1007/s10974-010-9204-y
M3 - Review article
C2 - 20195710
AN - SCOPUS:77951022683
SN - 0142-4319
VL - 30
SP - 243
EP - 253
JO - Journal of Muscle Research and Cell Motility
JF - Journal of Muscle Research and Cell Motility
IS - 7-8
ER -