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Glucocorticoid-induced muscle atrophy is characterized by fast-twitch or type II muscle fiber atrophy illustrated by decreased fiber cross-sectional area and reduced myofibrillar protein content. Muscle proteolysis, in particular through the ubiquitin— proteasome system UPS , is considered to play a major role in the catabolic action of glucocorticoids. Glucocorticoids also exert an anti-anabolic action by blunting muscle protein synthesis.
These changes in protein turnover may result from changes in the production of two growth factors which control muscle mass, namely IGF-I and myostatin respectively anabolic and catabolic toward the skeletal muscle.
The decreased production of IGF-I as well as the increased production of myostatin have been both demonstrated to contribute to the muscle atrophy caused by glucocorticoids. These recent progress in the understanding of the glucocorticoid-induced muscle atrophy should allow to define new therapies aiming to minimize this myopathy.
Promising new therapeutic approaches for treating glucocorticoid-induced muscle atrophy are also presented in this review. The catabolic effects of glucocorticoids have been well known for many years. Either as drugs used to treat several medical conditions or as endocrine hormones released in response to many stress situations, glucocorticoids may cause skeletal muscle atrophy.