Evidence map›Paper›PMID 22134166›Full record

ArticleBlood2012

Platelet TGF-β1 contributions to plasma TGF-β1, cardiac fibrosis, and systolic dysfunction in a mouse model of pressure overload.

Alexander Meyer, Wei Wang, Jiaxiang Qu, Lori Croft, Jay L Degen, Barry S Coller, Jasimuddin Ahamed

Open access · greenAbstract 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 115 papers.

0numbers the graph read from it
0cells of the map it votes in
115citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

115 citing papers in PubMed, 195 citations in OpenAlex.

  1. Trial
  2. Thromborepair: the tissue repair partner to thromboinflammation.Blood vessels, thrombosis & hemostasis · 2026
    Review
  3. Translational biology of human cardiac fibrosis.Nature cardiovascular research · 2026
    Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. CD4Frontiers in immunology · 2025
    Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. Article

55 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

7 authors at 4 institutions in 1 country.

Alexander MeyerLaboratory of Blood and Vascular Biology, Rockefeller University, 1230 York Ave., New York, NY 10065, USA.
Wei Wang
Jiaxiang Qu
Lori Croft
Jay L Degen
Barry S Coller
Jasimuddin Ahamed
Rockefeller University · USCincinnati Children's Hospital Medical Center · USMount Sinai Medical Center · USNew York University · US

Funding

TRANSFORMING TRANSLATIONAL SCIENCE AND EDUCATION TO BENEFIT HUMAN HEALTHUL1RR024143 · NCRR · ROCKEFELLER UNIVERSITY · PI COLLER, BARRY · 2006 to 2011
$49.1M
Platelet Integrin AlphaIIbBeta3 Structure, Activation, and Ligand Binding: Fibrinogen, Fibrin, D-dimer, and von Willebrand FactorR01HL019278 · NHLBI · STATE UNIVERSITY NEW YORK STONY BROOK · PI Claudia Lorena Buitrago, Barry Coller · 1985 to 2026
$17.6M
Hemostatic Factors as Determinants of Bacterial Virulence and Host Defense.R01HL085357 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI DEGEN, JAY L · 2006 to 2010
$1.8M
NCRR NIH HHS 5UL1RR024143NCRR NIH HHS UL1 RR024143NHLBI NIH HHS HL085357NHLBI NIH HHS R01 HL019278NHLBI NIH HHS R01 HL085357
6 · The paper itself

Abstract

Circulating platelets contain high concentrations of TGF-β1 in their α-granules and release it on platelet adhesion/activation. We hypothesized that uncontrolled in vitro release of platelet TGF-β1 may confound measurement of plasma TGF-β1 in mice and that in vivo release and activation may contribute to cardiac pathology in response to constriction of the transverse aorta, which produces both high shear and cardiac pressure overload. Plasma TGF-β1 levels in blood collected from C57Bl/6 mice by the standard retro-bulbar technique were much higher than those obtained when prostaglandin E₁ was added to inhibit release or when blood was collected percutaneously from the left ventricle under ultrasound guidance. Even with optimal blood drawing, plasma TGF-β1 was lower in mice rendered profoundly thrombocytopenic or mice with selectively low levels of platelet TGF-β1 because of megakaryocyte-specific disruption of their TGF-β1 gene (Tgfb1(flox)). Tgfb1(flox) mice were also partially protected from developing cardiac hypertrophy, fibrosis, and systolic dysfunction in response to transverse aortic constriction. These studies demonstrate that plasma TGF-β1 levels can be assessed accurately, but it requires special precautions; that platelet TGF-β1 contributes to plasma levels of TGF-β1; and that platelet TGF-β1 contributes to the pathologic cardiac changes that occur in response to aortic constriction.

Indexed as

AlprostadilAnimalsBlood PlateletsBlood VesselsCrosses, GeneticDisease Models, AnimalFibrosisHeartHemorrhageHypertensionIntegrasesMegakaryocytesMiceMice, Inbred C57BLMice, TransgenicMyocardiumAlprostadilCre recombinaseIntegrasesTgfb1 protein, mouseTransforming Growth Factor beta1

Identifiers

PMID22134166
PMCPMC3271718
OpenAlexW2055998280

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.