ArticleHuman molecular genetics2010
Flt-1 haploinsufficiency ameliorates muscular dystrophy phenotype by developmentally increased vasculature in mdx mice.
Article in Human molecular genetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 56 citations in OpenAlex.
- Developmental Cellular Programming: stage-specific architecting muscle and adipose tissues for high-quality meat production.Journal of animal science and biotechnology · 2026Review
- Deficiency of muscular dystrophy-related gene JAG2 causes NOTCH signaling dysfunction in muscle stem cells.The Journal of clinical investigation · 2026Article
- Article
- Cellular interactions and microenvironment dynamics in skeletal muscle regeneration and disease.Frontiers in cell and developmental biology · 2024Review
- miRNA-126a plays important role in myoblast and endothelial cell interaction.Scientific reports · 2023Article
- Restricted feeding regimens improve white striping associated muscular defects in broiler chickens.Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2023Article
- Vascular therapy for Duchenne muscular dystrophy (DMD).Faculty reviews · 2023Review
- Therapeutic Potential of Dental Pulp Stem Cells According to Different Transplant Types.Molecules (Basel, Switzerland) · 2021Review
- Dystrophin deficiency impairs vascular structure and function in the canine model of Duchenne muscular dystrophy.The Journal of pathology · 2021Article
- VEGFR-1/Flt-1 inhibition increases angiogenesis and improves muscle function in a mouse model of Duchenne muscular dystrophy.Molecular therapy. Methods & clinical development · 2021Article
- Age-Dependent Dysregulation of Muscle Vasculature and Blood Flow Recovery after Hindlimb Ischemia in theBiomedicines · 2021Article
- PTEN Inhibition Ameliorates Muscle Degeneration and Improves Muscle Function in a Mouse Model of Duchenne Muscular Dystrophy.Molecular therapy : the journal of the American Society of Gene Therapy · 2021Article
- Evolving Roles of Muscle-Resident Fibro-Adipogenic Progenitors in Health, Regeneration, Neuromuscular Disorders, and Aging.Frontiers in physiology · 2021Review
- Inhibition of FLT1 ameliorates muscular dystrophy phenotype by increased vasculature in a mouse model of Duchenne muscular dystrophy.PLoS genetics · 2019Article
- Review
- miR-146a deficiency does not aggravate muscular dystrophy in mdx mice.Skeletal muscle · 2019Article
- Inhibition of microRNA-92a increases blood vessels and satellite cells in skeletal muscle but does not improve duchenne muscular dystrophy-related phenotype in mdx mice.Muscle & nerve · 2019Article
- Targeting angiogenesis in Duchenne muscular dystrophy.Cellular and molecular life sciences : CMLS · 2019Review
- Isometric resistance training increases strength and alters histopathology of dystrophin-deficient mouse skeletal muscle.Journal of applied physiology (Bethesda, Md. : 1985) · 2019Article
- Tempol treatment shows phenotype improvement in mdx mice.PloS one · 2019Article
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Authors and funding
10 authors at 5 institutions in 3 countries.
Funding
Abstract
Duchenne muscular dystrophy (DMD) is an X-linked recessive genetic disease caused by mutations in the gene coding for the protein dystrophin. Recent work demonstrates that dystrophin is also found in the vasculature and its absence results in vascular deficiency and abnormal blood flow. This induces a state of ischemia further aggravating the muscular dystrophy pathogenesis. For an effective form of therapy of DMD, both the muscle and the vasculature need to be addressed. To reveal the developmental relationship between muscular dystrophy and vasculature, mdx mice, an animal model for DMD, were crossed with Flt-1 gene knockout mice to create a model with increased vasculature. Flt-1 is a decoy receptor for vascular endothelial growth factor, and therefore both homozygous (Flt-1(-/-)) and heterozygous (Flt-1(+/-)) Flt-1 gene knockout mice display increased endothelial cell proliferation and vascular density during embryogenesis. Here, we show that Flt-1(+/-) and mdx:Flt-1(+/-) adult mice also display a developmentally increased vascular density in skeletal muscle compared with the wild-type and mdx mice, respectively. The mdx:Flt-1(+/-) mice show improved muscle histology compared with the mdx mice with decreased fibrosis, calcification and membrane permeability. Functionally, the mdx:Flt-1(+/-) mice have an increase in muscle blood flow and force production, compared with the mdx mice. Consequently, the mdx:utrophin(-/-):Flt-1(+/-) mice display improved muscle histology and significantly higher survival rates compared with the mdx:utrophin(-/-) mice, which show more severe muscle phenotypes than the mdx mice. These data suggest that increasing the vasculature in DMD may ameliorate the histological and functional phenotypes associated with this disease.
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