Evidence map›Paper›PMID 33898634›Full record

ArticleMolecular therapy. Methods & clinical development2021

VEGFR-1/Flt-1 inhibition increases angiogenesis and improves muscle function in a mouse model of Duchenne muscular dystrophy.

Jennifer Bosco, Zhiwei Zhou, Sofie Gabriëls, Mayank Verma, Nan Liu, Brian K Miller, Sheng Gu, Dianna M Lundberg, Yan Huang, Eilish Brown and 10 more

Open access · goldAbstract read
In one paragraph

Article in Molecular therapy. Methods & clinical development, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.0field-weighted citation impact, top 26% 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

14 citing papers in PubMed, 15 citations in OpenAlex.

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  10. 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
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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

20 authors at 3 institutions in 2 countries.

Jennifer BoscoShire Human Genetic Therapies, a Takeda company, Lexington, MA, USA.
Zhiwei ZhouShire Human Genetic Therapies, a Takeda company, Lexington, MA, USA.
Sofie Gabriëlsargenx BVBA, Zwijnaarde, Belgium.
Mayank VermaStem Cell Institute, Paul and Sheila Wellstone Muscular Dystrophy Center, Department of Neurology, University of Minnesota Medical School, Minneapolis, MN, USA.
Nan LiuShire Human Genetic Therapies, a Takeda company, Lexington, MA, USA.
Brian K MillerShire Human Genetic Therapies, a Takeda company, Lexington, MA, USA.
Sheng GuShire Human Genetic Therapies, a Takeda company, Lexington, MA, USA.
Dianna M LundbergShire Human Genetic Therapies, a Takeda company, Lexington, MA, USA.
Yan HuangShire Human Genetic Therapies, a Takeda company, Lexington, MA, USA.
Eilish BrownShire Human Genetic Therapies, a Takeda company, Lexington, MA, USA.
Serene JosiahShire Human Genetic Therapies, a Takeda company, Lexington, MA, USA.
Muthuraman MeiyappanShire Human Genetic Therapies, a Takeda company, Lexington, MA, USA.
Matthew J TraylorShire Human Genetic Therapies, a Takeda company, Lexington, MA, USA.
Nancy ChenShire Human Genetic Therapies, a Takeda company, Lexington, MA, USA.
Atsushi AsakuraStem Cell Institute, Paul and Sheila Wellstone Muscular Dystrophy Center, Department of Neurology, University of Minnesota Medical School, Minneapolis, MN, USA.
Natalie De Jongeargenx BVBA, Zwijnaarde, Belgium.
Christophe Blanchetotargenx BVBA, Zwijnaarde, Belgium.
Hans de Haardargenx BVBA, Zwijnaarde, Belgium.
Heather S DuffyShire Human Genetic Therapies, a Takeda company, Lexington, MA, USA.
Dennis KeefeShire Human Genetic Therapies, a Takeda company, Lexington, MA, USA.
Takeda (United States) · USAblynx (Belgium) · BEUniversity of Minnesota · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Duchenne muscular dystrophy is characterized by structural degeneration of muscle, which is exacerbated by localized functional ischemia due to loss of nitric oxide synthase-induced vasodilation. Treatment strategies aimed at increasing vascular perfusion have been proposed. Toward this end, we have developed monoclonal antibodies (mAbs) that bind to the vascular endothelial growth factor (VEGF) receptor VEGFR-1 (Flt-1) and its soluble splice variant isoform (sFlt-1) leading to increased levels of free VEGF and proangiogenic signaling. The lead chimeric mAb, 21B3, had high affinity and specificity for both human and mouse sFlt-1 and inhibited VEGF binding to sFlt-1 in a competitive manner. Proof-of-concept studies in the

Indexed as

angiogenesisDuchenne muscular dystrophyfibrosismonoclonal antibodyvascular endothelial growth factor

Identifiers

PMID33898634
PMCPMC8055526
OpenAlexW3138565459

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.