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New IDRM research could pave the way for tackling muscle loss disorders

New research from the Wood and Rinaldi Labs has revealed a key interaction at the molecular level behind the maintenance of skeletal muscle homeostasis. This could lead to the identification of a new therapeutic target for treating acute and chronic conditions characterised by muscle atrophy.

AR cooperates with SMAD4 to maintain skeletal muscle homeostasis - Carlo Rinaldi.jpg
Image Credit: Carlo Rinaldi


Skeletal muscle accounts for more than 40% of the total mass in healthy individuals, and plays a vital role in maintaining homeostasis in the body. Muscle atrophy, caused by a range of conditions such as genetic muscular dystrophy, achexia and sarcopenia, is well known to correlate with levels of disability and as an important predictor of mortality. However, presently there are few treatments that can successfully counteract muscle loss due to an incomplete understanding of the underlying molecular mechanisms at play.

A team led by Associate Professor Carlo Rinaldi have elucidated a critical molecular mechanism of muscle homeostasis, where Androgen Receptor (AR) cooperates to orchestrate a muscle hypertrophy programme, forming a transcriptional complex with the SMAD4 protein in response to conditions of increased demand, such as physical exercise, denervation, and cachexia. They discovered that in spinal and bulbar muscular atrophy (SBMA), a genetic neuromuscular disease caused by a polyglutamine expansion (polyQ) in AR, this cooperative ability is lost, resulting in the severe primary muscle weakness and atrophy observed in affected individuals. 

Read the full story on the Department of Paediatrics website.

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