Vivo-Morpholinos: Same oligos, from cultures to critters -


Cellular and molecular mechanisms of muscle atrophy
Paolo Bonaldo, Marco Sandri


Skeletal muscle is a plastic organ that is maintained by multiple pathways regulating cell and protein turnover. During muscle atrophy, proteolytic systems are activated, and contractile proteins and organelles are removed, resulting in the shrinkage of muscle fibers. Excessive loss of muscle mass is associated with poor prognosis in several diseases, including myopathies and muscular dystrophies, as well as in systemic disorders such as cancer, diabetes, sepsis and heart failure. Muscle loss also occurs during aging. In this paper, we review the key mechanisms that regulate the turnover of contractile proteins and organelles in muscle tissue, and discuss how impairments in these mechanisms can contribute to muscle atrophy. We also discuss how protein synthesis and degradation are coordinately regulated by signaling pathways that are influenced by mechanical stress, physical activity, and the availability of nutrients and growth factors. Understanding how these pathways regulate muscle mass will provide new therapeutic targets for the prevention and treatment of muscle atrophy in metabolic and neuromuscular diseases.



    Our work is supported by grants from Telethon-Italy (GGP10225 and GGP11082 to P.B.; TCP04009 to M.S.), from the European Union (MYOAGE, contract: 223576 of FP7 to M.S.; BIO-NMD FP7-HEALTH-241665 to P.B.), ERC (MyoPHAGY to M.S.), the Italian Ministry of Education, University and Research (to P.B. and M.S.) and CARIPARO (to M.S. and P.B.).

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial Share Alike License (, which permits unrestricted non-commercial use, distribution and reproduction in any medium provided that the original work is properly cited and all further distributions of the work or adaptation are subject to the same Creative Commons License terms.

View Full Text