Study summary · research use only
Integrated expression analysis of muscle hypertrophy identifies Asb2 as a negative regulator of muscle mass
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
In this mouse study, follistatin-based interventions modulating the transforming growth factor-β (TGF-β) signaling network were reported to promote muscle hypertrophy that lessened aging-associated muscle wasting, though muscles of old sarcopenic mice showed a reduced response to follistatin compared with healthy young-adult muscle. Quantitative proteomic and transcriptomic analysis of young-adult muscles identified a transcription/translation signature triggered by follistatin exposure, including repression of ankyrin repeat and SOCS box protein 2 (Asb2). Increasing ASB2 expression was reported to reduce muscle mass, and sarcopenic muscles did not show reduced ASB2 abundance with follistatin exposure, while preventing ASB2 repression in young-adult muscles diminished follistatin-induced muscle hypertrophy. The authors state these findings identify Asb2 as a TGF-β network-responsive regulator of muscle mass.
Abstract
The transforming growth factor-β (TGF-β) signaling network is a critical regulator of skeletal muscle mass and function and, thus, is an attractive therapeutic target for combating muscle disease, but the underlying mechanisms of action remain undetermined. We report that follistatin-based interventions (which modulate TGF-β network activity) can promote muscle hypertrophy that ameliorates aging-associated muscle wasting. However, the muscles of old sarcopenic mice demonstrate reduced response to follistatin compared with healthy young-adult musculature. Quantitative proteomic and transcriptomic analyses of young-adult muscles identified a transcription/translation signature elicited by follistatin exposure, which included repression of ankyrin repeat and SOCS box protein 2 (Asb2). Increasing expression of ASB2 reduced muscle mass, thereby demonstrating that Asb2 is a TGF-β network-responsive negative regulator of muscle mass. In contrast to young-adult muscles, sarcopenic muscles do not exhibit reduced ASB2 abundance with follistatin exposure. Moreover, preventing repression of ASB2 in young-adult muscles diminished follistatin-induced muscle hypertrophy. These findings provide insight into the program of transcription and translation events governing follistatin-mediated adaptation of skeletal muscle attributes and identify Asb2 as a regulator of muscle mass implicated in the potential mechanistic dysfunction between follistatin-mediated muscle growth in young and old muscles.
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