Evidence map›Paper›PMID 24600399›Full record

ReviewFrontiers in physiology2014

Angiogenesis as a novel therapeutic strategy for Duchenne muscular dystrophy through decreased ischemia and increased satellite cells.

Yuko Shimizu-Motohashi, Atsushi Asakura

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Estrogen-related Receptor Signaling in Skeletal Muscle Fitness.International journal of sports medicine · 2023
    Article
  10. Article
  11. PI(4,5)PScience advances · 2023
    Article
  12. Re-examination of therapeutic management of muscular dystrophies using a vascular smooth muscle-centered approach.Journal of smooth muscle research = Nihon Heikatsukin Gakkai kikanshi · 2023
    Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. HIF-hypoxia signaling in skeletal muscle physiology and fibrosis.Journal of cell communication and signaling · 2020
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Yuko Shimizu-MotohashiStem 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.
Atsushi AsakuraStem 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.
University of Minnesota · US

Funding

Muscular Dystrophy Therapy by Increased AngiogenesisR03AR061545 · NIAMS · UNIVERSITY OF MINNESOTA · PI ASAKURA, ATSUSHI · 2012 to 2014
$221k
NIAMS NIH HHS R03 AR061545
6 · The paper itself

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.

Indexed as

angiogenesisFlt-1mdx micemuscular dystrophyregenerationsatellite cellskeletal muscleVEGF

Identifiers

PMID24600399
PMCPMC3927135
OpenAlexW2119036595

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.