*Corresponding author:Monica Canepari, Department of Molecular Medicine and Interuniversity Institute of Myology University of Pavia, Italy
Received:October 06, 2018; Published: October 15, 2018
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Steroid myopathy is a consequence of glucocorticoid administration and excess occurring in Cushing’s syndrome. It is characterized by muscle weakness, which impairs patients’ capacity to perform everyday activities. The relevance of steroid myopathy is very high especially given the large number of patients suffering from inflammatory diseases that are treated with glucocorticoids. The major pathogenetic mechanisms hypothesized are: imbalance between protein synthesis and degradation, impairment of mitochondrial function and redox imbalance. The triggers of the latter phenomena and muscle damage are still unknown. The latter issues are still unsatisfactorily settled mainly because analyses are mostly focused at times when steroid myopathy had fully developed making it difficult to take apart the phenomena causing the myopathy from those being a consequence of it. To identify the triggering mechanisms involved in the pathogenesis of steroid myopathy the very early stages of the phenomenon must be investigated. This short review describes the effect of short-term corticosteroid administration on muscle functional, structural and molecular adaptations in humans and mice.
Keywords :Steroid Myopathy; Glucocorticoids; Muscle Atrophy; Dexamethasone
Abbreviations : Akt: Protein Kinase B; CSA: Cross-Sectional Area; DEX: Dexamethasone; FoxO: Fork-Head Box O; mTOR: Mammalian Target of Rapamycin; MuRF-1: Muscle-Specific Ring Finger Protein-1; NRF2: Nuclear Factor (Erythroid-Derived 2)-Like2 (Nre2l2); PGC-1α: Peroxisome Proliferative Activated Receptor-Γ Coactivator 1α; Po/CSA: Specific Force; SD: Standard Deviation; Sol: Soleus Muscle; SOD1: Cu/Zn Superoxide Dismutase; UPS: Ubiquitin Proteasome System; VL: Vastus Lateralis Muscle