Evidence map›Paper›PMID 31624779›Full record

ReviewResearch and practice in thrombosis and haemostasis2019

Factor XII - What's important but not commonly thought about.

Alvin H Schmaier, Evi X Stavrou

Open access · goldAbstract readReview
In one paragraph

Review in Research and practice in thrombosis and haemostasis, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
3.9field-weighted citation impact, top 6% 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

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

  1. Factor XII-A New Therapeutic Target? A Systematic Review.International journal of molecular sciences · 2026
    Pooled it
  2. Article
  3. Trypsin is as procoagulant as factor XIIa.Bleeding, thrombosis and vascular biology · 2026
    Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Observational
  10. Article
  11. Review
  12. Article
  13. Triazol-1-yl Benzamides Promote Anticoagulant ActivityCardiovascular & hematological agents in medicinal chemistry · 2023
    Article
  14. Review
  15. Review
  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

2 authors at 2 institutions in 1 country.

Alvin H SchmaierDepartment of Medicine Case Western Reserve University Cleveland Ohio.
Evi X StavrouDepartment of Medicine Case Western Reserve University Cleveland Ohio.
University Hospitals of Cleveland · USVA Northeast Ohio Healthcare System · US

Funding

Contact Pathway Activation on Vascular DevicesR01HL144113 · NHLBI · OREGON HEALTH & SCIENCE UNIVERSITY · PI HINDS, MONICA T, MCCARTY, OWEN J · 2018 to 2025
$6.0M
Kruppel-Like Factor 2 Counters Vascular and Immunologic Dysfunction in Child Cerebral MalariaR01AI130131 · NIAID · CASE WESTERN RESERVE UNIVERSITY · PI KAZURA, JAMES WALTER · 2017 to 2021
$3.0M
Targeted Abrogation of the FXII-uPAR-pAkt2 Axis in Neutrophils for Treatment of Chronic WoundsR01HL137695 · NHLBI · CASE WESTERN RESERVE UNIVERSITY · PI STAVROU, EVI X. · 2019 to 2023
$2.0M
BLRD VA I01 BX003851NHLBI NIH HHS R01 HL137695NHLBI NIH HHS R01 HL144113NIAID NIH HHS R01 AI130131
6 · The paper itself

Abstract

Factor XII (FXII) becomes a serine protease when blood is exposed to artificial medical surfaces or when pathologic surfaces arise in disease states leading to its autoactivation. Initiation of the blood coagulation cascade was the first recognized activity of FXIIa. Blocking FXIIa activity formed on artificial medical surfaces should reduce induced blood coagulation leading to thrombosis. In contrast to FXII enzymatic activities, less is known about zymogen FXII functions. Studies show that zymogen FXII has biologic activity in various cells in vivo. In endothelium, FXII stimulates cell growth and proliferation and, in vivo, neoangiogenesis after injury. In fibroblasts, transforming growth factor-β increases FXII expression, which in turn stimulates fibroblast proliferation, contributing to tissue fibrosis. In neutrophils, FXII stimulates Akt2 to initiate neutrophil adhesion, migration, and chemotaxis, priming events leading to NETosis. Factor FXII deficiency leads to decreased neutrophil recruitment and improved wound healing. In dendritic cells, FXII contributes to neuroinflammation, and its deficiency or pharmacologic inhibition renders mice less susceptible to autoimmune encephalomyelitis. These combined studies indicate that FXII also contributes to multiple components of the inflammatory response. In sum, targeting FXII's biologic activities may provide novel approaches to reduce thrombosis and the inflammatory response in various disease states.

Indexed as

C1 inhibitorcontact activationfactor XIIhigh‐molecular‐weight kininogenprekallikreinurokinase plasminogen activator receptor

Identifiers

PMID31624779
PMCPMC6781921
OpenAlexW2949851679

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.