As Wnt activity increases during aging, muscle cell progenitors switch from a myogenic (i.e., regenerative) mode to a fibrogenic (i.e., inflammatory) mode; this can be prevented with specific blocking antibodies. It is easy to that the resulting increased fibrogenesis, at the cost of regenerative capacity, could cause muscular weakness and sarcopenia in late life.
Here's a few thoughts from elsewhere in the blogosphere a couple of weeks ago:
What does this mean for us? Well, if you block the wnt pathway you could very well promote tissue healing. The truism that you heal slower when you're older would no longer hold true. More interesting however is that many of the obvious signs of aging are due to imperfect cellular maintenance--what if selective wnt pathway suppression could change that? The wnt pathway is crucial so this is something that you're want to only block on a selective basis but it's a very interesting area of research.
This latest round of Wnt-related discussion has focused on aging and cancer, but the last round was all regeneration.
vertebrate regeneration is under the control of the powerful Wnt signaling system: Activating it overcomes the mysterious barrier to regeneration in animals like chicks that can't normally replace missing limbs while inactivating it in animals known to be able to regenerate their limbs (frogs, zebrafish, and salamanders) shuts down their ability to replace missing legs and tails. ... In this simple experiment, we removed part of the chick embryo's wing, activated Wnt signaling, and got the whole limb back - a beautiful and perfect wing
mice have retained incipient potential for continuous tooth generation and that it can be unlocked by activating Wnt signalling. It is reasonable to conjecture that the potential for continuous tooth generation may also have been retained in humans
We've found that we can influence wound healing with wnts or other proteins that allow the skin to heal in a way that has less scarring and includes all the normal structures of the skin, such as hair follicles and oil glands, rather than just a scar ... By introducing more wnt proteins to the wound, the researchers found that they could take advantage of the embryonic genes to promote hair-follicle growth, thus making skin regenerate instead of just repair. Conversely by blocking wnt proteins, they also found that they could stop the production of hair follicles in healed skin.
Human biochemistry is packed with systems like this - vital and influential in regeneration, cancer, aging and other equally important processes and systems. Biology is complex in ways that only an evolved system can be; evolution encourages reuse and multiple purposes for the same component. That in turn leads to balances and trade-offs in longevity, health and evolutionary fitness.
More importantly for us, this complexity makes reengineering our biochemistry a tough job indeed; we're only just getting started, and it's already enough to keep the bulk of the world's medical research community occupied. They won't be finished up any time soon. That's one of the reasons I believe repair strategies like SENS to be a far superior path forward to healthy life extension. Don't struggled through the endless morass of bringing change to the complex systems of our biology: rather, learn how those systems work, and how to repair the specific types of damage that lead to aging. That's a monster of a job in and of itself, but a job that can be achieved rapidly enough to benefit those reading this today.