title: Cellular mechanisms and local progenitor activation to regulate skeletal muscle mass.
abstract: 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.
authors.affiliation: Translational Cardiomyology, SCIL Katholieke Universiteit Leuven, Herestraat 49 bus 814, Leuven 3000, Belgium.
authors.forename: Marco
authors.initials: M
authors.lastname: Cassano
authors.forename: Mattia
authors.initials: M
authors.lastname: Quattrocelli
authors.forename: Stefania
authors.initials: S
authors.lastname: Crippa
authors.forename: Ilaria
authors.initials: I
authors.lastname: Perini
authors.forename: Flavio
authors.initials: F
authors.lastname: Ronzoni
authors.forename: Maurilio
authors.initials: M
authors.lastname: Sampaolesi
mesh_terms: D000818:Animals; D001284:Atrophy / Q000378:metabolism / Q000473:pathology; D002100:Cachexia / Q000378:metabolism / Q000473:pathology; D002454:Cell Differentiation / Q000502:physiology*; D002477:Cells / Q000378:metabolism; D005786:Gene Expression Regulation; D006801:Humans; D006984:Hypertrophy / Q000378:metabolism / Q000473:pathology; D024510:Muscle Development; D018482:Muscle, Skeletal / Q000166:cytology* / Q000378:metabolism* / Q000473:pathology; D009132:Muscles / Q000378:metabolism; D009133:Muscular Atrophy / Q000378:metabolism / Q000473:pathology; D009135:Muscular Diseases / Q000378:metabolism / Q000473:pathology; D009141:Musculoskeletal System / Q000378:metabolism; D032446:Myoblasts / Q000378:metabolism; D055435:Myostatin / Q000378:metabolism; D012038:Regeneration / Q000502:physiology; D013002:Somatomedins / Q000378:metabolism*
chemical_list: D055435:Myostatin; D013002:Somatomedins