February 28, 2008

Tendons May Need Myostatin to Stay Supple

Blocking the protein myostatin as a possible way of increasing muscle mass and strength has been a goal of clinical and laboratory research in the muscular dystrophies for several years. However, new results from the University of Michigan reveal a previously unrecognized downside of myostatin blocking.

John Faulkner and colleagues, who published their results Jan. 8 in Proceedings of the National Academy of Sciences, have found that mice bred to lack myostatin from birth have tendons that are 14 times stiffer than tendons in mice that produce myostatin.

Tendons attach muscles to bone, and their flexibility plays a role in protecting muscle fibers from contraction-associated injuries. Muscle fibers in boys with Duchenne muscular dystrophy (DMD) are particularly susceptible to this type of injury.

It isn’t yet known whether myostatin blocking has the same effect on human tendons as it does on mouse tendons, or whether blocking myostatin months to years after birth would be different from stopping its production before birth. However, the findings are a caveat about strategies to block myostatin as a treatment for muscular dystrophy.