The possible role of myostatin in skeletal muscle atrophy and cachexia

The presence of sufficient skeletal muscle is of paramount importance for body function. Cachexia can be defined as a wasting syndrome describing the progressive loss of both adipose and skeletal muscle tissue in concert with severe injury, chronic or end-stage malignant and infectious diseases. Generally, cachexia predisposes to poor prognosis, co-morbidities and death. One signaling pathway possibly involved in muscle atrophy and cachexia is the myostatin cascade. This transforming growth factor-beta superfamily member myostatin is a strong candidate for regulating muscle mass, and is shown to inhibit muscle growth in different in vivo mammalian models. Overall, the modulation of the myostatin pathway seems interesting from the perspective of both pathology and sports medicine. Hence, myostatin signaling components and post-translational modulators are possible targets of pharmacological and other treatments against muscle loss, thus potentially contributing to the understanding and mitigation of muscle atrophies associated with inactivity, senescence and disease.