Evidence map›Paper›PMID 16684956›Full record

ArticleBlood2006

The thrombospondin-1 N700S polymorphism is associated with early myocardial infarction without altering von Willebrand factor multimer size.

Jeffrey I Zwicker, Flora Peyvandi, Roberta Palla, Rossana Lombardi, Maria Teresa Canciani, Andrea Cairo, Diego Ardissino, Luisa Bernardinelli, Kenneth A Bauer, Jack Lawler and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

24 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Thrombospondin-1 in maladaptive aging responses: a concept whose time has come.American journal of physiology. Cell physiology · 2020
    Review
  6. Review
  7. THBS1 (thrombospondin-1).Atlas of genetics and cytogenetics in oncology and haematology · 2020
    Article
  8. Article
  9. Thrombospondins: A Role in Cardiovascular Disease.International journal of molecular sciences · 2017
    Review
  10. Polymorphisms in host genes encoding NOSII, C-reactive protein, and adhesion molecules thrombospondin and E-selectin are risk factors for Plasmodium falciparum malaria in India.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2015
    Article
  11. Association ofBiomedical reports · 2015
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Review
  20. Thrombospondin-1 and CD47 regulate blood pressure and cardiac responses to vasoactive stress.Matrix biology : journal of the International Society for Matrix Biology · 2009
    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

11 authors at 1 institution in 2 countries.

Jeffrey I ZwickerDepartment of Pathology, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA. jzwicker@bidmc.harvard.edu
Flora Peyvandi
Roberta Palla
Rossana Lombardi
Maria Teresa Canciani
Andrea Cairo
Diego Ardissino
Luisa Bernardinelli
Kenneth A Bauer
Jack Lawler
Pier Mannucci
Istituti di Ricovero e Cura a Carattere Scientifico · IT

Funding

NHLBI NIH HHS HL6803
6 · The paper itself

Abstract

The N700S polymorphism of thrombospondin-1 (TSP-1) has been identified as a potential genetic risk factor for myocardial infarction (MI). In a large case-control study of 1425 individuals who survived a myocardial infarction prior to age 45, the N700S polymorphism was a significant risk factor for myocardial infarction in both homozygous (odds ratio [OR] 1.9, 95% confidence interval [CI] 1.1-3.3, P = .01) and heterozygous carriers of the S700 allele (OR 1.4, 95% CI 1.1-3.3, P = .01). TSP-1 has been shown to reduce von Willebrand factor (VWF) multimer size, and the domain responsible for VWF-reducing activity has been localized to the calcium-binding C-terminal sequence. As the N700S polymorphism was previously shown to alter the function of this domain, we investigated whether the altered VWF-reducing activity of TSP-1 underlies the observed prothrombotic phenotype. The TSP1 N700S polymorphism did not influence VWF multimer size in patients homozygous for either allele nor was there a significant reduction of VWF multimer size following incubation with recombinant N700S fragments or platelet-derived TSP-1.

Indexed as

Genetic Predisposition to DiseasePolymorphism, Single NucleotideAllelesCase-Control StudiesDisease-Free SurvivalFemaleHeterozygoteHumansMaleMyocardial InfarctionProtein BindingProtein Structure, TertiaryRisk FactorsThrombospondin 1von Willebrand FactorThrombospondin 1von Willebrand Factor

Identifiers

PMID16684956
PMCPMC1895875
OpenAlexW2133788189

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.