ArticleExperimental and therapeutic medicine2018
Adeno-associated virus serotype 9 mediated vascular endothelial growth factor gene overexpression in mdx mice.
Article in Experimental and therapeutic medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- Genetic strategies for therapy of Duchenne muscular dystrophy.Molecular therapy. Nucleic acids · 2025Review
- 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
- Inhibition of FLT1 ameliorates muscular dystrophy phenotype by increased vasculature in a mouse model of Duchenne muscular dystrophy.PLoS genetics · 2019Article
- Targeting angiogenesis in Duchenne muscular dystrophy.Cellular and molecular life sciences : CMLS · 2019Review
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Duchenne muscular dystrophy (DMD) is a fatal neuromuscular disease caused by the absence of dystrophin. Vascular endothelial growth factor (VEGF) is a heparin-binding dimeric glycoprotein and principal angiogenic factor stimulating the migration, proliferation and expression of various genes in endothelial cells. Recently, VEGF was demonstrated to exhibit an antiapoptotic and direct myogenic effect, as well as to enhance muscle force restoration subsequent to traumatic injury. Therefore, the present study attempted to assess the muscle damage of VEGF overexpression in mdx mice. Adeno-associated virus serotype 9 (AAV9)-VEGF was administered intravenously to mdx mice. At 4 weeks after injection, VEGF was observed to be upregulated in the tibialis anterior muscle. In addition, the serum creatine kinase levels were significantly reduced and fatigue was slowed down, whereas the limb grip strength and weight of mice were markedly increased compared with the saline-treated mdx mice. Furthermore, significantly reduced inflammation and necrosis areas were observed in the muscle tissues of mice in the AAV9-VEGF group. These results suggested that AAV9-mediated VEGF gene overexpression was able to improve the muscle damage in mdx mice.
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