Evidence map›Paper›PMID 12426405›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2002

Tissue factor deficiency causes cardiac fibrosis and left ventricular dysfunction.

R Pawlinski, A Fernandes, B Kehrle, B Pedersen, G Parry, J Erlich, R Pyo, D Gutstein, J Zhang, F Castellino and 7 more

Open access · greenAbstract readComparative Study
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

37 citing papers in PubMed, 100 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review
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

17 authors at 1 institution in 1 country.

R PawlinskiDepartment of Immunology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.
A Fernandes
B Kehrle
B Pedersen
G Parry
J Erlich
R Pyo
D Gutstein
J Zhang
F Castellino
E Melis
P Carmeliet
G Baretton
T Luther
M Taubman
E Rosen
N Mackman
TU Dresden · DE

Funding

VASCULAR MOLECULAR AND CELLS BIOLOGYP01HL016411 · NHLBI · SCRIPPS RESEARCH INSTITUTE, THE · PI RUF, WOLFRAM · 1985 to 2008
$21.5M
BLOOD COAGULATION PROTEIN-METAL ION-LIPID INTERACTIONSR01HL019982 · NHLBI · UNIVERSITY OF NOTRE DAME · PI CASTELLINO, FRANCIS J · 1985 to 2013
$4.9M
BLOOD COAGULATION &FIBRINOLYSISR01HL065226 · NHLBI · SCRIPPS RESEARCH INSTITUTE · PI MACKMAN, NIGEL · 2000 to 2004
$1.8M
NHLBI NIH HHS HL19982NHLBI NIH HHS P01 HL016411NHLBI NIH HHS P01 HL16411NHLBI NIH HHS R01 HL019982NHLBI NIH HHS R01 HL065226NHLBI NIH HHS R01 HL65226
6 · The paper itself

Abstract

Exposure of blood to tissue factor (TF) activates the extrinsic (TF:FVIIa) and intrinsic (FVIIIa:FIXa) pathways of coagulation. In this study, we found that mice expressing low levels of human TF ( approximately 1% of wild-type levels) in an mTF(-/-) background had significantly shorter lifespans than wild-type mice, in part, because of spontaneous fatal hemorrhages. All low-TF mice exhibited a selective heart defect that consisted of hemosiderin deposition and fibrosis. Direct intracardiac measurement demonstrated a 30% reduction (P < 0.001) in left ventricular function in 8-month-old low-TF mice compared with age-matched wild-type mice. Mice expressing low levels of murine FVII ( approximately 1% of wild-type levels) exhibited a similar pattern of hemosiderin deposition and fibrosis in their hearts. In contrast, FIX(-/-) mice, a model of hemophilia B, had normal hearts. Cardiac fibrosis in low-TF and low-FVII mice appears to be caused by hemorrhage from cardiac vessels due to impaired hemostasis. We propose that TF expression by cardiac myocytes provides a secondary hemostatic barrier to protect the heart from hemorrhage.

Indexed as

AnimalsEndomyocardial FibrosisFactor VIIFibrinogenGene ExpressionGenetic Predisposition to DiseaseHemophilia BHemorrhagic DisordersHemosiderinHemostasisHumansMiceMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutMice, TransgenicFactor VIIFibrinogenHemosiderinRecombinant Fusion ProteinsThromboplastin

Identifiers

PMID12426405
PMCPMC137717
OpenAlexW1650396825

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.