Evidence map›Paper›PMID 23125197›Full record

ReviewCold Spring Harbor perspectives in medicine2012

Common polymorphisms in angiogenesis.

Michael S Rogers, Robert J D'Amato

Open access · bronzeAbstract readReview
In one paragraph

Review in Cold Spring Harbor perspectives in medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
–field-weighted citation impact
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

12 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. A unique finding of the basilar artery.Surgical and radiologic anatomy : SRA · 2021
    Article
  7. Article
  8. Article
  9. Article
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  11. Article
  12. Genetic modification of corneal neovascularization in Dstn (corn1) mice.Mammalian genome : official journal of the International Mammalian Genome Society · 2013
    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

2 authors at 2 institutions in 1 country.

Michael S RogersVascular Biology Program, Children's Hospital, Boston, Massachusettes, USA. michael.rogers@childrens.harvard.edu
Robert J D'Amato
Boston Children's Hospital · USHarvard University · US

Funding

Identification of Common Polymorphisms Affecting AngiogenesisR01EY012726 · NEI · CHILDREN'S HOSPITAL BOSTON · PI D'AMATO, ROBERT J · 1999 to 2015
$5.0M
NEI NIH HHS R01 EY012726
6 · The paper itself

Abstract

A wide variety of diseases have a significant genetic component, including major causes of morbidity and mortality in the western world. Many of these diseases are also angiogenesis dependent. In humans, common polymorphisms, although more subtle in effect than rare mutations that cause Mendelian disease, are expected to have greater overall effects on human disease. Thus, common polymorphisms in angiogenesis-regulating genes may affect the response to an angiogenic stimulus and thereby affect susceptibility to or progression of such diseases. Candidate gene studies have identified several associations between angiogenesis gene polymorphisms and disease. Similarly, emerging pharmacogenomic evidence indicates that several angiogenesis-regulating polymorphisms may predict response to therapy. In contrast, genome-wide association studies have identified only a few risk alleles in obvious angiogenesis genes. As in other traits, regulatory polymorphisms appear to dominate the landscape of angiogenic responsiveness. Rodent assays, including the mouse corneal micropocket assay, tumor models, and a macular degeneration model have allowed the identification and comparison of loci that directly affect the trait. Complementarity between human and animal approaches will allow increased understanding of the genetic basis for angiogenesis-dependent disease.

Indexed as

Polymorphism, GeneticAnimalsGene Expression RegulationGenome-Wide Association StudyHumansHypoxia-Inducible Factor 1, alpha SubunitIntegrinsInterleukin-8Neovascularization, PathologicNitric Oxide Synthase Type IIIPeptide HydrolasesQuantitative Trait LociTissue Inhibitor of MetalloproteinasesVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-2Hypoxia-Inducible Factor 1, alpha SubunitIntegrinsInterleukin-8Nitric Oxide Synthase Type IIIPeptide HydrolasesTissue Inhibitor of MetalloproteinasesVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-2

Identifiers

PMID23125197
PMCPMC3543099
OpenAlexW2165881188

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.