Grant: Project Grant

While there is a strong association between osteoporosis and skeletal muscle atrophy/dysfunction, the functional relevance of a particular biological pathway that synchronously regulates bone and skeletal muscle physiopathology had remained elusive. Our research team shows that a regulator of bone remodeling, osteoprotegerin (OPG), completely rescues fast-twitch skeletal muscles, protects against cardiac hypertrophy and improves glucose metabolism in a mouse model of Duchenne muscular dystrophy (DMD). OPG treatments also enhance force production and reduce muscle damage in a mouse model of congenital muscular dystrophy (CMD). This research shows a mutual cross-talk between bone-heart-skeletal muscle-metabolism which should translate into clinical results for patients with DMD or CMD and possibly other muscle diseases. We have high hopes that our research will lead to new disease-modifying treatments that will make it possible to restore the function of dystrophic muscles without correcting the dystrophin gene.