Research suggests that the receptor may be a good target for new drugs to treat a variety of muscle disorders and injuries.
When injuries are severe — with more than 20 percent loss of muscle mass — normal muscle regeneration often cannot keep pace with the regenerative demands. In this scenario, the loss of skeletal muscle mass can trigger widespread fibrosis and loss of muscle function.
Eventually, muscle regeneration may become unable to keep up, even with assistance through dietary interventions, anabolic steroids or non-steroidal anti-inflammatories (NSAIDs). The use of anabolic steroids and NSAIDs are accompanied by severe side effects that may further reduce the quality of life. Often, pharmacological interventions fail to stem long-term decline in quality of life or enhance survival for those with degenerative muscle tissue diseases.
“Identifying new means of accelerating muscle regeneration has proved a daunting challenge,” Burris said. “Therefore understanding the underlying mechanisms that regulate muscle cell regeneration and coordinate regenerative repair could provide future therapeutic options for stymieing the loss of muscle function in the traumatically injured.”
Successful regeneration of skeletal muscle after traumatic injury depends on the replenishment of muscle fibers through elevated myoblast proliferation and differentiation.
Scientists were fascinated to see that REV-ERB appears to play different roles for different stages of muscle tissue development. A decline in expression of REV-ERB precedes myoblast differentiation. Conversely, an increase in REV-ERB expression is involved in the regulation of mitochondrial and metabolic function in fully differentiated skeletal muscle.
The research team identified a mechanism through which REV-ERB may regulate gene expression pre and post muscle differentiation. They show that REV-ERB is a regulator of muscle differentiation that can be targeted to stimulate muscle regeneration and may be useful in treating numerous muscle diseases, including muscular dystrophy, sarcopenia, and cachexia, in addition to acute injury.