Duchenne muscular dystrophy (DMD) is a severe hereditary disease characterized 
by the absence of dystrophin on the sarcolemma of muscle fiber. This absence 
results in widespread muscle damage and satellite cell activation. After 
depletion of the satellite cell pool, skeletal muscle is then invariably 
replaced by connective tissue, leading to progressive muscle weakness. Herein, 
we isolated Flk-1(+) mesenchymal stem cells (MSCs) from adult adipose tissue and 
induced them to differentiate into skeletal muscle cells in culture. Within mdx 
mice, an animal model of DMD, adipose tissue-derived Flk-1(+) MSCs (AD-MSCs) 
homed to and differentiated into cells that repaired injured muscle tissue. This 
repair correlated with reconstitution of dystrophin expression on the damaged 
fibers. Flk-1(+) AD-MSCs also differentiated into muscle satellite cells. This 
differentiation may have accounted for long-term reconstitution. These cells 
also differentiated into endothelial cells, thereby possibly improving fiber 
regeneration as a result of the induced angiogenesis. Therefore, Flk-1(+) AD-MSC 
transplants may repair muscular dystrophy.