The possible role of myostatin in skeletal muscle atrophy and cachexia

[Guest guest]

Scand J Med Sci Sports. 2006 Apr;16(2):74-82.

The possible role of myostatin in skeletal muscle atrophy and

cachexia.

Jespersen J, Kjaer M, Schjerling P.

Institute of Sports Medicine, Bispebjerg Hospital, Copenhagen,

Denmark.

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.