Evidence map›Paper›PMID 27207433›Full record

ReviewThrombosis research2016

The hemostatic role of factor XI.

Cristina Puy, Rachel A Rigg, Owen J T McCarty

Open access · greenAbstract readReview
In one paragraph

Review in Thrombosis research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 9% 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

50 citing papers in PubMed, 1 synthesis or guideline pooled it, 85 citations in OpenAlex.

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

3 authors at 1 institution in 1 country.

Cristina PuyDepartment of Biomedical Engineering, School of Medicine, Oregon Health & Science University, Portland, OR, United States; Division of Hematology and Medical Oncology, School of Medicine, Oregon Health & Science University, Portland, OR, United States. Electronic address: puygarci@ohsu.edu.
Rachel A RiggDepartment of Biomedical Engineering, School of Medicine, Oregon Health & Science University, Portland, OR, United States.
Owen J T McCartyDepartment of Biomedical Engineering, School of Medicine, Oregon Health & Science University, Portland, OR, United States; Division of Hematology and Medical Oncology, School of Medicine, Oregon Health & Science University, Portland, OR, United States.
Oregon Health & Science University · US

Funding

Characterization of Coagulation Factor-platelet Interactions: Role of FXIR01HL101972 · NHLBI · OREGON HEALTH & SCIENCE UNIVERSITY · PI Owen J McCarty · 2010 to 2026
$8.5M
FXI and SepsisR01GM116184 · NIGMS · OREGON HEALTH & SCIENCE UNIVERSITY · PI LUPU, FLOREA, MCCARTY, OWEN J · 2015 to 2018
$1.9M
NHLBI NIH HHS R01 HL101972NIGMS NIH HHS R01 GM116184
6 · The paper itself

Abstract

Coagulation factor (F)XI has been described as a component of the early phase of the contact pathway of blood coagulation, acting downstream of factor XII. However, patients deficient in upstream members of the contact pathway, including FXII and prekallikrein, do not exhibit bleeding complications, while FXI-deficient patients sometimes experience mild bleeding, suggesting FXI plays a role in hemostasis independent of the contact pathway. Further complicating the picture, bleeding risk in FXI-deficient patients is difficult to predict because bleeding symptoms have not been found to correlate with FXI antigen levels or activity. However, recent studies have emerged to expand our understanding of FXI, demonstrating that activated FXI is able to activate coagulation factors FX, FV, and FVIII, and inhibit the anti-coagulant tissue factor pathway inhibitor (TFPI). Understanding these activities of FXI may help to better diagnose which FXI-deficient patients are at risk for bleeding. In contrast to its mild hemostatic activities, FXI is known to play a significant role in thrombosis, as it is a demonstrated independent risk factor for deep vein thrombosis, ischemic stroke, and myocardial infarction. Recent translational approaches have begun testing FXI as an antithrombotic, with one promising clinical study showing that an anti-sense oligonucleotide against FXI prevented venous thrombosis in elective knee surgery. A better understanding of the varied and complex role of FXI in both thrombosis and hemostasis will help to allow better prediction of bleeding risk in FXI-deficient patients and also informing the development of targeted agents to inhibit the thrombotic activities of FXI while preserving hemostasis.

Indexed as

HemostasisAnimalsAnticoagulantsBlood CoagulationDrug DiscoveryFactor XIFactor XI DeficiencyHemorrhageHumansThrombosisAnticoagulantsFactor XIbleedingcoagulation factor XIcoagulation factor XIIcontact activation pathwayhemophilia Chemostasis

Identifiers

PMID27207433
PMCPMC6135087
OpenAlexW2401721742

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.