Evidence map›Paper›PMID 16533887›Full record

ArticleThe Journal of experimental medicine2006

Targeting coagulation factor XII provides protection from pathological thrombosis in cerebral ischemia without interfering with hemostasis.

Christoph Kleinschnitz, Guido Stoll, Martin Bendszus, Kai Schuh, Hans-Ulrich Pauer, Peter Burfeind, Christoph Renné, David Gailani, Bernhard Nieswandt, Thomas Renné

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The Journal of experimental medicine, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 179 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
179citing papers in PubMed, 1 pooled it
11.1field-weighted citation impact, top 1% 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

179 citing papers in PubMed, 1 synthesis or guideline pooled it, 446 citations in OpenAlex.

  1. Pooled it
  2. Review
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  11. Article
  12. Article
  13. Factor XII-driven coagulation traps bacterial infections.The Journal of experimental medicine · 2025
    Article
  14. Article
  15. Review
  16. Factor XI: structure, function and therapeutic inhibition.Journal of thrombosis and thrombolysis · 2024
    Review
  17. Article
  18. The third-generation anticoagulants: factors XI, XII, and XIII inhibitors.The Egyptian heart journal : (EHJ) : official bulletin of the Egyptian Society of Cardiology · 2024
    Review
  19. Article
  20. Review

119 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 4 institutions in 2 countries.

Christoph KleinschnitzDepartment of Neurology, Institute for Clinical Biochemistry and Pathobiochemistry, University of Würzburg, 97080 Würzburg, Germany.
Guido Stoll
Martin Bendszus
Kai Schuh
Hans-Ulrich Pauer
Peter Burfeind
Christoph Renné
David Gailani
Bernhard Nieswandt
Thomas Renné
University of Würzburg · DEGoethe University Frankfurt · DEUniversity of Göttingen · DEVanderbilt University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Formation of fibrin is critical for limiting blood loss at a site of blood vessel injury (hemostasis), but may also contribute to vascular thrombosis. Hereditary deficiency of factor XII (FXII), the protease that triggers the intrinsic pathway of coagulation in vitro, is not associated with spontaneous or excessive injury-related bleeding, indicating FXII is not required for hemostasis. We demonstrate that deficiency or inhibition of FXII protects mice from ischemic brain injury. After transient middle cerebral artery occlusion, the volume of infarcted brain in FXII-deficient and FXII inhibitor-treated mice was substantially less than in wild-type controls, without an increase in infarct-associated hemorrhage. Targeting FXII reduced fibrin formation in ischemic vessels, and reconstitution of FXII-deficient mice with human FXII restored fibrin deposition. Mice deficient in the FXII substrate factor XI were similarly protected from vessel-occluding fibrin formation, suggesting that FXII contributes to pathologic clotting through the intrinsic pathway. These data demonstrate that some processes involved in pathologic thrombus formation are distinct from those required for normal hemostasis. As FXII appears to be instrumental in pathologic fibrin formation but dispensable for hemostasis, FXII inhibition may offer a selective and safe strategy for preventing stroke and other thromboembolic diseases.

Indexed as

HemostasisAnimalsBlood Coagulation Factor InhibitorsBlood VesselsBrain IschemiaFactor XI DeficiencyFactor XIIFactor XII DeficiencyFemaleFibrinMaleMiceMice, KnockoutThrombosisBlood Coagulation Factor InhibitorsFactor XIIFibrin

Identifiers

PMID16533887
PMCPMC2118228
OpenAlexW2107916818

What OpenQuestion holds

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LicenceCC BY-NC-SA
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.