Evidence map›Paper›PMID 23006890›Full record

ReviewJournal of thrombosis and haemostasis : JTH2012

Regulation of tissue factor coagulant activity on cell surfaces.

L V M Rao, U R Pendurthi

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of thrombosis and haemostasis : JTH, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 1 pooled it
5.6field-weighted citation impact, top 4% 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

48 citing papers in PubMed, 1 synthesis or guideline pooled it, 107 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Is anticoagulative therapy in systemic sclerosis to be reconsidered?Journal of scleroderma and related disorders · 2024
    Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. Review
  15. Role of Mesenchymal Stem/Stromal Cells in Coagulation.International journal of molecular sciences · 2022
    Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. 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 1 institution in 1 country.

L V M RaoDepartment of Cellular and Molecular Biology, Center for Biomedical Research, The University of Texas Health Science Center, Tyler, TX, USA.
U R Pendurthi
The University of Texas Health Science Center at Tyler · US

Funding

Factor VIIa Interaction with Endothelial Cell Protein C ReceptorR01HL107483 · NHLBI · UNIVERSITY OF TEXAS HLTH CTR AT TYLER · PI LELLA, VIJAYA MOHAN RAO · 2012 to 2019
$2.9M
INITIATION AND REGULATION OF BLOOD COAGULATIONR01HL058869 · NHLBI · UNIVERSITY OF TEXAS HLTH CTR AT TYLER · PI LELLA, VIJAYA MOHAN RAO · 1998 to 2010
$2.3M
Tissue Factor-factor Vlla signalingR01HL065500 · NHLBI · UNIVERSITY OF TEXAS HLTH CTR AT TYLER · PI PENDURTHI, USHA R · 2001 to 2010
$1.8M
NHLBI NIH HHS HL1074830NHLBI NIH HHS HL58869NHLBI NIH HHS HL65500NHLBI NIH HHS R01 HL058869NHLBI NIH HHS R01 HL065500NHLBI NIH HHS R01 HL107483
6 · The paper itself

Abstract

Tissue factor (TF) is a transmembrane glycoprotein and an essential component of the factor VIIa-TF enzymatic complex that triggers activation of the coagulation cascade. Formation of TF-FVIIa complexes on cell surfaces not only trigger the coagulation cascade but also transduce cell signaling via activation of protease-activated receptors. Tissue factor is expressed constitutively on cell surfaces of a variety of extravascular cell types, including fibroblasts and pericytes in and surrounding blood vessel walls and epithelial cells, but is generally absent on cells that come into contact with blood directly. However, TF expression could be induced in some blood cells, such as monocytes and endothelial cells, following an injury or pathological stimuli. Tissue factor is essential for hemostasis, but aberrant expression of TF leads to thrombosis. Therefore, a proper regulation of TF activity is critical for the maintenance of hemostatic balance and health in general. TF-FVIIa coagulant activity at the cell surface is influenced not only by TF protein expression levels but also independently by a variety of mechanisms, including alterations in membrane phospholipid composition and cholesterol content, thiol-dependent modifications of TF allosteric disulfide bonds, and other post-translational modifications of TF. In this article, we critically review the key literature on mechanisms by which TF coagulant activity is regulated at the cell surface in the absence of changes in TF protein levels with specific emphasis on recently published data and provide the authors' perspective on the subject.

Indexed as

Gene Expression RegulationAllosteric SiteAnimalsCaveolaeCell MembraneCholesterolCoagulantsDisulfidesFibroblastsGlycosylationHemostasisHumansMembrane MicrodomainsPericytesPhospholipidsProtein Disulfide-IsomerasesCholesterolCoagulantsDisulfidesPhospholipidsProtein Disulfide-IsomerasesSulfhydryl CompoundsThromboplastincholesterolcrypticdecryptionencryptionfactor VIIaglycosylationphospholipidsprotein disulfide isomerasetissue factor

Identifiers

PMID23006890
PMCPMC3558600
OpenAlexW1954611773

What OpenQuestion holds

Textmetadata
LicenceTDM
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.