More On Myostatin and Satellite Cells in the Aging Body
You might recall work from earlier this year on the reduction in stem cell capabilities with aging; it suggested that stem cell populations decline, but their ability to regenerate does not. This contracts other research that suggests just the opposite; it should be interesting to see just how these results are reconciled in the end. Head to head contradictions are a strong sign of a field in flux and progress, carving understanding from the rock face of the unknown. At the present pace of stem cell research, we'll have an answer before the end of 2008.
Ouroboros pointed out a more recent paper that takes the "lots of stem cells, but declining ability to regenerate" side of the debate. This one also ties into myostatin and the promotion of muscle growth, something that has been put forward as a potential path to therapies for sarcopenia, or age-related muscle loss.
In young mice, lack of myostatin resulted in increased satellite cell number and activation compared to wild-type, suggesting a greater propensity to undergo myogenesis, a difference maintained in the aged mice. In addition, muscle regeneration of myostatin-null muscle following notexin injury was accelerated and fiber hypertrophy and type were recovered with regeneration, unlike in wild-type muscle. In conclusion, a lack of myostatin appears to reduce age-related sarcopenia and loss of muscle regenerative capacity.
This makes sense; you need active stem cells to grow muscle. So what is myostatin doing with the satellite stem cell population associated with muscle growth and repair? Answering that question might go a long way towards understanding what causes our stem cells to decline in activity with increasing age - and then to move on to safely preventing that fate.
Technorati tags: aging, stem cell research
Negative regulation is a consistent paradigm in cellular signaling. There are numerous control and check points that prevent energy expensive and uncontrolled proliferation (like cancer) processes. Myostatin appears to support an evolutionary pathway whose primary directive is energy conservation. Maintaining muscle bulk requires more calories than adipose tissue and does not yield much functional advantage (even though many strength athletes may beg to differ). It is interesting, however, that the default pathway is for muscle development and that by resistance training (or other stimulus) the levels of myostatin are reduced and the underlying signaling to develop muscle are permitted to operate.