The study identifies two ubiquitin ligases, Muscle RING Finger 1 (MuRF1) and Muscle Atrophy F-box (MAFbx), as key mediators of skeletal muscle atrophy. Through transcript profiling, the researchers found that only a small subset of genes was universally upregulated across multiple atrophy models. Over-expression of MAFbx in myotubes induced atrophy, while mice deficient in either MAFbx or MuRF1 were resistant to atrophy. These findings suggest that MAFbx and MuRF1 are potential novel drug targets for treating muscle atrophy. The study also highlights the importance of these proteins in maintaining muscle mass and their potential roles in cardiac muscle remodeling and disease.The study identifies two ubiquitin ligases, Muscle RING Finger 1 (MuRF1) and Muscle Atrophy F-box (MAFbx), as key mediators of skeletal muscle atrophy. Through transcript profiling, the researchers found that only a small subset of genes was universally upregulated across multiple atrophy models. Over-expression of MAFbx in myotubes induced atrophy, while mice deficient in either MAFbx or MuRF1 were resistant to atrophy. These findings suggest that MAFbx and MuRF1 are potential novel drug targets for treating muscle atrophy. The study also highlights the importance of these proteins in maintaining muscle mass and their potential roles in cardiac muscle remodeling and disease.