Evidence map›Paper›PMID 34125270›Full record

ReviewSeminars in immunopathology2021

The contact system in liver injury.

Chandini Rangaswamy, Reiner K Mailer, Hanna Englert, Sandra Konrath, Thomas Renné

Open access · hybridAbstract readReview
In one paragraph

Review in Seminars in immunopathology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.4field-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

20 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Research and practice in thrombosis and haemostasis · 2025
    Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Combined oral contraceptives may activate the contact system in healthy women.Research and practice in thrombosis and haemostasis · 2023
    Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Mediators of liver inflammation and carcinogenesis.Seminars in immunopathology · 2021
    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

5 authors at 1 institution in 1 country.

Chandini RangaswamyInstitute of Clinical Chemistry and Laboratory Medicine (O26), University Medical Center Hamburg-Eppendorf, Martinistrasse 52, D-20246, Hamburg, Germany.
Reiner K MailerInstitute of Clinical Chemistry and Laboratory Medicine (O26), University Medical Center Hamburg-Eppendorf, Martinistrasse 52, D-20246, Hamburg, Germany.ORCID 0000-0001-8279-3355
Hanna EnglertInstitute of Clinical Chemistry and Laboratory Medicine (O26), University Medical Center Hamburg-Eppendorf, Martinistrasse 52, D-20246, Hamburg, Germany.
Sandra KonrathInstitute of Clinical Chemistry and Laboratory Medicine (O26), University Medical Center Hamburg-Eppendorf, Martinistrasse 52, D-20246, Hamburg, Germany.
Thomas RennéInstitute of Clinical Chemistry and Laboratory Medicine (O26), University Medical Center Hamburg-Eppendorf, Martinistrasse 52, D-20246, Hamburg, Germany. thomas@renne.net.
Universität Hamburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Coagulation is controlled by a delicate balance of prothrombotic and antithrombotic mechanisms, to prevent both excessive blood loss from injured vessels and pathologic thrombosis. The liver plays a pivotal role in hemostasis through the synthesis of plasma coagulation factors and their inhibitors that, in addition to thrombosis and hemostasis, orchestrates an array of inflammatory responses. As a result, impaired liver function has been linked with both hypercoagulability and bleeding disorders due to a pathologic balance of pro- and anticoagulant plasma factors. At sites of vascular injury, thrombus propagation that finally may occlude the blood vessel depends on negatively charged biopolymers, such as polyphosphates and extracellular DNA, that provide a physiological surface for contact activation of coagulation factor XII (FXII). FXII initiates the contact system that drives both the intrinsic pathway of coagulation, and formation of the inflammatory mediator bradykinin by the kallikrein-kinin system. Moreover, FXII facilitates receptor-mediated signalling, thereby promoting mitogenic activities, angiogenesis, and neutrophil stimulation with implications for liver diseases. Here, we summarize current knowledge on the FXII-driven contact system in liver diseases and review therapeutic approaches to target its activities during impaired liver function.

Indexed as

Factor XIIThrombosisBlood CoagulationHumansKallikrein-Kinin SystemLiverFactor XIICoagulationContact systemFactor XIIInflammationLiver disease

Identifiers

PMID34125270
PMCPMC8202222
OpenAlexW3171414115

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.