Despite the incredible capacity of skeletal muscle for self-repair and regeneration following injury, a variety of congenital disorders, acquired diseases, and traumatic injuries result in irrecoverable loss of muscle function. Key among these is VML injury, characterized by a degree of muscle tissue absence or loss that exceeds the endogenous regenerative capacity of muscle, resulting in permanent functional and cosmetic deficits. Such injuries affect both the military and civilian populations. Current treatment for VML injuries is limited to surgical muscle transfers of autologous or allogenic muscle, and these treatments are associated with both poor engraftment at the host site and morbidity at the donor site. As such, there is currently no effective therapeutic option for treatment of VML injuries.