title: Angiogenesis as a novel therapeutic strategy for Duchenne muscular dystrophy through decreased ischemia and increased satellite cells.
abstract: Duchenne muscular dystrophy (DMD) is the most common hereditary muscular dystrophy caused by mutation in dystrophin, and there is no curative therapy. Dystrophin is a protein which forms the dystrophin-associated glycoprotein complex (DGC) at the sarcolemma linking the muscle cytoskeleton to the extracellular matrix. When dystrophin is absent, muscle fibers become vulnerable to mechanical stretch. In addition to this, accumulating evidence indicates DMD muscle having vascular abnormalities and that the muscles are under an ischemic condition. More recent studies demonstrate decreased vascular densities and impaired angiogenesis in the muscles of murine model of DMD. Therefore, generation of new vasculature can be considered a potentially effective strategy for DMD therapy. The pro-angiogenic approaches also seem to be pro-myogenic and could induce muscle regeneration capacity through expansion of the satellite cell juxtavascular niche in the mouse model. Here, we will focus on angiogenesis, reviewing the background, vascular endothelial growth factor (VEGF)/VEGF receptor-pathway, effect, and concerns of this strategy in DMD.
authors.affiliation: Stem Cell Institute, University of Minnesota Medical School Minneapolis, MN, USA ; Paul and Sheila Wellstone Muscular Dystrophy Center, University of Minnesota Medical School Minneapolis, MN, USA ; Department of Neurology, University of Minnesota Medical School Minneapolis, MN, USA.
authors.forename: Yuko
authors.initials: Y
authors.lastname: Shimizu-Motohashi
authors.affiliation: Stem Cell Institute, University of Minnesota Medical School Minneapolis, MN, USA ; Paul and Sheila Wellstone Muscular Dystrophy Center, University of Minnesota Medical School Minneapolis, MN, USA ; Department of Neurology, University of Minnesota Medical School Minneapolis, MN, USA.
authors.forename: Atsushi
authors.initials: A
authors.lastname: Asakura
keywords: Flt-1; VEGF; angiogenesis; mdx mice; muscular dystrophy; regeneration; satellite cell; skeletal muscle