Muscle atrophy has been associated with bone loss, but the muscle-derived signals that regulate bone metabolism remain largely unknown. A study published in Science Translational Medicine identifies the adaptor protein FNIP1 as a mediator of the muscle–bone crosstalk.

This study started with the observation that bone mineral density (BMD) is reduced in paediatric patients with limb-girdle muscular dystrophy (LGMD). “Numerous studies have shown a close association between muscle dysfunction and the development of bone diseases. Conversely, exercise is effective in improving muscle function and thereby influences bone remodelling, leading to enhanced bone health. However, diminished mechanical loading alone is unlikely to fully explain the bone loss seen in several muscle atrophies,” notes Zhenji Gan, co-corresponding author of the study. Li, Zhu, Gan and colleagues thus screened for differentially expressed genes in dystrophic skeletal muscles that might contribute to bone loss.