Glucocorticoid-Induced Muscle Atrophy: Insights And Therapies
Okorie Uchechukwu,
Nweke Timothy Obinna,
Ofodile Vitus Anayo,
Okorie Loveth Onyekachi
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.
