Evidence map›Paper›PMID 26090874›Full record

ArticleGene therapy2015

Inhibition of pathological brain angiogenesis through systemic delivery of AAV vector expressing soluble FLT1.

F Shen, L Mao, W Zhu, M T Lawton, P Pechan, P Colosi, Z Wu, A Scaria, H Su

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Gene therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

5 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
  2. VEGFR1 as a Target for Cardiovascular Gene Therapy.Journal of cardiovascular translational research · 2025
    Review
  3. Article
  4. Article
  5. Article
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

9 authors at 4 institutions in 2 countries.

F ShenCenter for Cerebrovascular Research, Department of Anesthesia and Perioperative Care, University of California, San Francisco, San Francisco, CA, USA.
L MaoCenter for Cerebrovascular Research, Department of Anesthesia and Perioperative Care, University of California, San Francisco, San Francisco, CA, USA.
W ZhuCenter for Cerebrovascular Research, Department of Anesthesia and Perioperative Care, University of California, San Francisco, San Francisco, CA, USA.
M T LawtonDepartment of Neurological Surgery, University of California, San Francisco, San Francisco, CA, USA.
P PechanSanofi-Genzyme R&D Center, Framingham, MA, USA.
P ColosiOcular Gene Therapy Core, National Eye Institute, National Institutes of Health, Bethesda, MD, USA.
Z WuOcular Gene Therapy Core, National Eye Institute, National Institutes of Health, Bethesda, MD, USA.
A ScariaSanofi-Genzyme R&D Center, Framingham, MA, USA.
H SuCenter for Cerebrovascular Research, Department of Anesthesia and Perioperative Care, University of California, San Francisco, San Francisco, CA, USA.
University of California, San Francisco · USNational Institutes of Health · USNeurological Surgery · USRuijin Hospital · CN

Funding

Uncover the Pathogenesis of Brain Arteriovenous MalformationR01NS027713 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI SU, HUA · 1990 to 2023
$8.6M
Retinal Gene TherapyZIAEY000443 · NEI · NATIONAL EYE INSTITUTE · PI LI, TIANSEN · 2009 to 2020
$8.4M
Cell type-specific influences on HHT pathogenesisR01HL122774 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI SU, HUA · 2015 to 2018
$1.6M
Soluble VEGF receptor therapy for brain arteriovenous malformationR21NS083788 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI SU, HUA · 2014 to 2015
$790k
Targeted Gene Expression in Ischemic Brain by Intravenous DeliveryR21NS070153 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI SU, HUA · 2010 to 2011
$382k
NHLBI NIH HHS R01 HL122774NINDS NIH HHS R01 NS027713NINDS NIH HHS R21 NS070153NINDS NIH HHS R21 NS083788
6 · The paper itself

Abstract

The soluble vascular endothelial growth factor (VEGF) receptor 1 (sFLT1) has been tested in both animals and humans for anti-angiogenic therapies, for example, age-related macular degeneration. We hypothesized that adeno-associated viral vector (AAV)-mediated sFLT1 expression could be used to inhibit abnormal brain angiogenesis. We tested the anti-angiogenic effect of sFLT1 and the feasibility of using AAV serotype 9 to deliver sFLT1 through intravenous injection (IV) to the brain angiogenic region. AAVs were packaged in AAV serotypes 1 and 2 (stereotactic injection) and 9 (IV injection). Brain angiogenesis was induced in adult mice through stereotactic injection of AAV1-VEGF. AAV2-sFLT02 containing sFLT1 VEGF-binding domain (domain 2) was injected into the brain angiogenic region, and AAV9-sFLT1 was injected into the jugular vein at the time of or 4 weeks after AAV1-VEGF injection. We showed that AAV2-sFLT02 inhibited brain angiogenesis at both time points. IV injection of AAV9-sFLT1 inhibited angiogenesis only when the vector was injected 4 weeks after angiogenic induction. Neither lymphocyte infiltration nor neuron loss was observed in AAV9-sFLT1-treated mice. Our data show that systemically delivered AAV9-sFLT1 inhibits angiogenesis in the mouse brain, which could be utilized to treat brain angiogenic diseases such as brain arteriovenous malformation.

Indexed as

Gene Transfer TechniquesAngiogenesis InhibitorsAnimalsBrainDependovirusGenetic TherapyGenetic VectorsMaleMiceMice, Inbred C57BLNeovascularization, PathologicRandom AllocationVascular Endothelial Growth Factor Receptor-1Angiogenesis InhibitorsFLT1 protein, humanVascular Endothelial Growth Factor Receptor-1

Identifiers

PMID26090874
PMCPMC4636448
OpenAlexW1553074396

What OpenQuestion holds

Textmetadata
LicenceTDM
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.