Developing a nutrient-based formulation to attenuate muscle wasting
Muscle atrophy causes weakness and disability in aging, inactivity, and in many diseases. This loss of muscle mass and strength is primarily due to the accelerated degradation of muscle proteins by the ubiquitin-proteasome system (UPS). The ubiquitin ligases, F-Box (MAFbx/Atrogin-1) and Muscle RING-Finger 1 (MuRF-1), are induced in most types of atrophy and currently represent the best markers for atrophy. Their expression increases also by the Transforming Growth Factor-β (TGF-β) family member, myostatin, which functions as a negative regulator of skeletal muscle mass. Myostatin is produced by muscle, and is excessively active in systemic catabolic conditions (including cancer cachexia and aging), causing a severe muscle atrophy. Its inhibition is currently considered as the best therapeutic approach to prevent or retard atrophy. Here we focus on the development of a nutrient-based formulation that specifically targets myostatin signaling for the treatment of muscle wasting in humans.