Angiogenic therapy for muscular dystrophy

Duchenne Muscular Dystrophy (DMD) is caused by mutations in the dystrophin gene, which normally functions to maintain muscle membrane integrity and prevent contraction‐induced damage. It may be possible to reduce muscle fiber damage by using pro‐angiogenic factors or endothelial progenitor cells to increase muscle perfusion and observe the resultant effects on the muscular dystrophy phenotype. We predict that these pro‐angiogenic factors and endothelial progenitor cells will assist in development of new therapies for DMD via increased vascular density in blood‐starved dystrophic muscles