期刊
JOURNAL OF CACHEXIA SARCOPENIA AND MUSCLE
卷 9, 期 7, 页码 1255-1268出版社
WILEY
DOI: 10.1002/jcsm.12363
关键词
Sarcopenia; S100B; Oxidative stress; Myoblast; Brown adipocyte; Myofiber
资金
- Association Francaise contre les Myopathies [12992, 16812]
- Associazione Italiana per la Ricerca sul Cancro [17581]
- Ministero dell'Istruzione, dell'Universita e della Ricerca, Italy [PRIN 2009WBFZYM_002, PRIN 2010R8JK2X_004, PRIN 2012N8YJC3, FIRB RBFR12BUMH]
- Fondazione Cassa di Risparmio di Perugia [2012.0241.021, 2015.0325.021, 2016-0136.021]
Primary sarcopenia is a condition of reduced skeletal muscle mass and strength, reduced agility, and increased fatigability and risk of bone fractures characteristic of aged, otherwise healthy people. The pathogenesis of primary sarcopenia is not completely understood. Herein, we review the essentials of the cellular and molecular mechanisms of skeletal mass maintenance; the alterations of myofiber metabolism and deranged properties of muscle satellite cells (the adult stem cells of skeletal muscles) that underpin the pathophysiology of primary sarcopenia; the role of the Ca2+-sensor protein, S100B, as an intracellular factor and an extracellular signal regulating cell functions; and the functional role of S100B in muscle tissue. Lastly, building on recent results pointing to S100B as to a molecular determinant of myoblast-brown adipocyte transition, we propose S100B as a transducer of the deleterious effects of accumulation of reactive oxygen species in myoblasts and, potentially, myofibers concurring to the pathophysiology of sarcopenia.
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