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development of muscle atrophy, in which a loss of muscle mass leads to muscle weakness. Thus, muscle atrophy is considered to be a prognostic factor for underlying diseases ( Schakman et al . 2013 ). Glucocorticoids cause muscle atrophy by upregulating the

difficulties, falls, and effects daily life activities ( Goodpaster et al. 2006 , Delmonico et al. 2007 ). It has also been reported that muscle atrophy increases the risk of death ( Cruz-Jentoft et al. 2010 ). The pathogenesis of skeletal muscle atrophy

that seem to be specifically involved in myofibrillar protein degradation, the mouse atrophy gene-1 (atrogin-1; Gomes et al. 2001 ), also described as the rat muscle atrophy F-box (MAFbx; Bodine et al. 2001 ), and the rat muscle RING finger-1

skeletal muscle atrophy. The resulting weakness of peripheral and respiratory muscles may have major clinical implications such as loss of quality of life, fatigue, impaired wound healing, compromised lung function, and poor immune response. The purpose of

. 2014 ). Low serum levels of vitamin D are known to be associated with reduced muscle strength and performance, and lead to muscle atrophy, increased apoptosis, decreased protein synthesis, and perturbation in intracellular calcium homeostasis ( Ceglia

inhibits dexamethasone-induced muscle atrophy in L6 cells ( Sundaram et al . 2009 ). The biological functions of E 2 are exerted through its binding to two estrogen receptors (ERs), ERα and ERβ ( Heldring et al . 2007 ). The ERs bind to estrogen response

muscle mass ( McClung et al . 2006 , Sitnick et al . 2006 , Sugiura et al . 2006 , Pollanen et al . 2011 ). Ovariectomized (OVX) mice fail to fully recover muscle mass after hindlimb suspension-induced muscle atrophy followed by reloading ( McClung

available myonuclei via inflammatory or apoptotic-like mechanisms represent alternative explanations for sarcopenia ( Leeuwenburgh 2003 ). Muscle atrophy in disuse, denervation and medical disorders Muscle atrophies with disuse, ageing

proteasome for hydrolysis ( Lecker et al . 2006 ). It is well established that GCs drive muscle atrophy through modulation of protein metabolism ( McGrath & Goldspink 1982 , Savary et al . 1998 , Biedasek et al . 2011 ). However, the precise molecular

side effects of systemic androgen therapy. As such, there is considerable interest in more targeted therapeutic options for treating muscle atrophy. Although androgenic effects on muscle are generally presumed to occur via actions on myocyte androgen