MSTN and osteogenesis imperfecta: By breeding heterozygote + /oim mice to heterozygote myostatin deficiency (+ /mstn) mice, the congenic double heterozygote (+ /mstn + /oim) mice displayed greater body weight, muscle mass, bone volume, and biomechanical strength than their + /oim littermates, indicating a likely role of myostatin deficiency in rescuing the defective muscle-bone unit and improving the mechanotransduction in OI condition.