Evidence map›Paper›PMID 36685169›Full record

ArticleFrontiers in physiology2022

Mutant plasminogen in hereditary angioedema is bypassing FXII/kallikrein to generate bradykinin.

Stefan Hintze, Britta S Möhl, Jessica Beyerl, Karin Wulff, Andreas Wieser, Konrad Bork, Peter Meinke

Open access · goldAbstract read
In one paragraph

Article in Frontiers in physiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
4.9field-weighted citation impact, top 5% 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

14 citing papers in PubMed, 17 citations in OpenAlex.

  1. Trial
  2. Article
  3. Garadacimab for the long-term prophylaxis of hereditary angioedema.Journal der Deutschen Dermatologischen Gesellschaft = Journal of the German Society of Dermatology : JDDG · 2026
    Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Status quo and future developments in the diagnosis and treatment of hereditary angioedema.Journal der Deutschen Dermatologischen Gesellschaft = Journal of the German Society of Dermatology : JDDG · 2025
    Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. 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

7 authors at 6 institutions in 1 country.

Stefan HintzeFriedrich-Baur-Institute at the Department of Neurology, University Hospital, Ludwig-Maximilians-University Munich, Munich, Germany.
Britta S MöhlInstitute of Virology, School of Medicine, Technical University of Munich/Helmholtz Zentrum München, Munich, Germany.
Jessica BeyerlDivision of Infectious Diseases and Tropical Medicine, University Hospital, Ludwig-Maximilians-University Munich, Munich, Germany.
Karin WulffUniversity Medicine, University of Greifswald, Greifswald, Germany.
Andreas WieserDivision of Infectious Diseases and Tropical Medicine, University Hospital, Ludwig-Maximilians-University Munich, Munich, Germany.
Konrad BorkDepartment of Dermatology, University Medical Center, Johannes Gutenberg University, Mainz, Germany.
Peter MeinkeFriedrich-Baur-Institute at the Department of Neurology, University Hospital, Ludwig-Maximilians-University Munich, Munich, Germany.
Fraunhofer Institute for Translational Medicine and Pharmacology · DEFriedrich Baur Stiftung · DEHelmholtz Zentrum München · DEJohannes Gutenberg University Mainz · DELudwig-Maximilians-Universität München · DEUniversität Greifswald · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hereditary angioedema (HAE) is characterized by recurrent localized edema in various organs, which can be potentially fatal. There are different types of hereditary angioedema, which include genetic deficiency of C1 inhibitor (C1-INH) and hereditary angioedema with normal C1-INH (HAEnCI). In HAEnCI patients mutations have been identified in the

Indexed as

bradykininFXIIHAE-PLGHereditary angioedema (HAE)kallikrein-kinin system (KKS)normal C1-INHplasminogen

Identifiers

PMID36685169
PMCPMC9849239
OpenAlexW4313576925

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.