TY  - JOUR
AU  - Okorie Uchechukwu
AU  - Nweke Timothy Obinna
AU  - Ofodile Vitus Anayo
AU  - Okorie Loveth Onyekachi
PY  - 2026
DA  - 2026/06/03
TI  - Glucocorticoid-Induced Muscle Atrophy: Insights And Therapies
JO  - Japan Journal of Research
VL  - 7
IS  - 4
AB  - 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.
SN  - 2690-8077
UR  - https://dx.doi.org/10.33425/2690-8077.1237
DO  - 10.33425/2690-8077.1237