Evidence map›Paper›PMID 23007403›Full record

ArticleBlood2012

Semaphorin 6A regulates angiogenesis by modulating VEGF signaling.

Marta Segarra, Hidetaka Ohnuki, Dragan Maric, Ombretta Salvucci, Xu Hou, Anil Kumar, Xuri Li, Giovanna Tosato

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

66 citing papers in PubMed, 95 citations in OpenAlex.

  1. Article
  2. Semaphorins and Their Role in Neuropathic Pain.Life (Basel, Switzerland) · 2026
    Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Semaphorin 6A phase separation sustains a histone lactylation-dependent lactate buildup in pathological angiogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  15. SEMA6A overexpression inhibited tumor growth and metastasis in colorectal cancer.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2025
    Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review

6 more citing papers are in PubMed but not listed here.

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

8 authors at 4 institutions in 1 country.

Marta SegarraLaboratory of Cellular Oncology, Center for Cancer Research, National Cancer Institute, National Institutes of Health (NIH), Bethesda MD 20892, USA.
Hidetaka Ohnuki
Dragan Maric
Ombretta Salvucci
Xu Hou
Anil Kumar
Xuri Li
Giovanna Tosato
Center for Cancer Research · USNational Eye Institute · USNational Institute of Neurological Disorders and Stroke · USNational Institutes of Health · US

Funding

Angiogenesis and Tumor GrowthZIASC010355 · NCI · DIVISION OF CLINICAL SCIENCES - NCI · PI TOSATO, GIOVANNA · 2009 to 2025
$13.3M
Intramural NIH HHS
6 · The paper itself

Abstract

Formation of new vessels during development and in the mature mammal generally proceeds through angiogenesis. Although a variety of molecules and signaling pathways are known to underlie endothelial cell sprouting and remodeling during angiogenesis, many aspects of this complex process remain unexplained. Here we show that the transmembrane semaphorin6A (Sema6A) is expressed in endothelial cells, and regulates endothelial cell survival and growth by modulating the expression and signaling of VEGFR2, which is known to maintain endothelial cell viability by autocrine VEGFR signaling. The silencing of Sema6A in primary endothelial cells promotes cell death that is not rescued by exogenous VEGF-A or FGF2, attributable to the loss of prosurvival signaling from endogenous VEGF. Analyses of mouse tissues demonstrate that Sema6A is expressed in angiogenic and remodeling vessels. Mice with null mutations of Sema6A exhibit significant defects in hyaloid vessels complexity associated with increased endothelial cell death, and in retinal vessels development that is abnormally reduced. Adult Sema6A-null mice exhibit reduced tumor, matrigel, and choroidal angiogenesis compared with controls. Sema6A plays important roles in development of the nervous system. Here we show that it also regulates vascular development and adult angiogenesis.

Indexed as

Signal TransductionAnimalsCell ProliferationCell SurvivalChoroidFibroblast Growth Factor 2Gene SilencingHumansHuman Umbilical Vein Endothelial CellsMiceMice, KnockoutNeovascularization, PhysiologicRetinaRetinal VesselsSemaphorinsVascular Endothelial Growth Factor AFibroblast Growth Factor 2Sema6a protein, mouseSemaphorinsVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-2

Identifiers

PMID23007403
PMCPMC3496961
OpenAlexW2025389449

What OpenQuestion holds

Textmetadata
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.