Abstract

Excess of glucocorticoid (Gs) due to diseases of the adrenal gland, stress, aging, and immunosuppressant use can induce muscle atrophy (loss of muscle mass). Gs plays a crucial role in muscle atrophy by decreasing protein synthesis and increasing its breakdown. The fundamental implication of excess glucocorticoids is the up-regulation of the atrophy-related genes atrogin1, MuRF1, and MUSA1. E3 ubiquitin ligases are typically muscular-specific catalyzing ubiquitination of target protein. Additionally, glucocorticoids increase the expression of parts of the Notch signaling pathway in muscle, activate a significant amount of UPS components that help conjugate a protein to be degraded, decrease the cellular level of MyoD, a transcription factor required for muscle mass development, and increase the production of Myostatin, a growth factor that is known to inhibit muscle mass development. IGF- 1 induction, myostatin inhibition, and cAMP phosphodiesterase inhibitors are examples of potential treatments to stop muscle atrophy brought on by glucocorticoids. Similarly, administration of androgens and branched-chain amino acids, particularly leucine could restore muscle atrophy. This review discussed glucocorticoid-induced muscle atrophy and therapeutic approaches.