Evidence map›Paper›PMID 35697739›Full record

ArticleScientific reports2022

Association of FXI activity with thrombo-inflammation, extracellular matrix, lipid metabolism and apoptosis in venous thrombosis.

Alejandro Pallares Robles, Vincent Ten Cate, Andreas Schulz, Jürgen H Prochaska, Steffen Rapp, Thomas Koeck, Marina Panova-Noeva, Stefan Heitmeier, Stephan Schwers, Kirsten Leineweber and 10 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
4.3field-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

22 citing papers in PubMed, 33 citations in OpenAlex.

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  8. Proteomic Insights into Venous Thromboembolism.Medical sciences (Basel, Switzerland) · 2026
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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

20 authors at 6 institutions in 3 countries.

Alejandro Pallares RoblesClinical Epidemiology and Systems Medicine, Center for Thrombosis and Hemostasis (CTH), University Medical Center of the Johannes Gutenberg University Mainz, 55131, Mainz, Germany.
Vincent Ten CateClinical Epidemiology and Systems Medicine, Center for Thrombosis and Hemostasis (CTH), University Medical Center of the Johannes Gutenberg University Mainz, 55131, Mainz, Germany.
Andreas SchulzPreventive Cardiology and Preventive Medicine, Center for Cardiology, University Medical Center of the Johannes Gutenberg University Mainz, 55131, Mainz, Germany.
Jürgen H ProchaskaClinical Epidemiology and Systems Medicine, Center for Thrombosis and Hemostasis (CTH), University Medical Center of the Johannes Gutenberg University Mainz, 55131, Mainz, Germany.
Steffen RappPreventive Cardiology and Preventive Medicine, Center for Cardiology, University Medical Center of the Johannes Gutenberg University Mainz, 55131, Mainz, Germany.
Thomas KoeckPreventive Cardiology and Preventive Medicine, Center for Cardiology, University Medical Center of the Johannes Gutenberg University Mainz, 55131, Mainz, Germany.
Marina Panova-NoevaClinical Epidemiology and Systems Medicine, Center for Thrombosis and Hemostasis (CTH), University Medical Center of the Johannes Gutenberg University Mainz, 55131, Mainz, Germany.
Stefan HeitmeierBayer AG, 42113, Wuppertal, Germany.
Stephan SchwersBayer AG, 42113, Wuppertal, Germany.
Kirsten LeineweberBayer AG, 42113, Wuppertal, Germany.
Hans-Jürgen SeyfarthDepartment of Pneumology, University of Leipzig, 4289, Leipzig, Germany.
Christian F OpitzDepartment of Cardiology, DRK-Kliniken Westend, 14050, Berlin, Germany.
Henri SpronkCardiovascular Research Institute Maastricht (CARIM), Maastricht University Medical Center, Maastricht, 6229 HB, The Netherlands.
Christine Espinola-KleinCenter for Cardiology - Cardiology I, University Medical Center, Johannes Gutenberg University Mainz, Mainz, 55131, Germany.
Karl J LacknerInstitute of Clinical Chemistry and Laboratory Medicine, University Medical Center of the Johannes Gutenberg University Mainz, 55131, Mainz, Germany.
Thomas MünzelCenter for Cardiology - Cardiology I, University Medical Center, Johannes Gutenberg University Mainz, Mainz, 55131, Germany.
Miguel A Andrade-NavarroInstitute of Organismic and Molecular Evolution, Johannes Gutenberg University Mainz, 55128, Mainz, Germany.
Stavros V KonstantinidesCenter for Thrombosis and Hemostasis (CTH), University Medical Center of the Johannes Gutenberg University Mainz, 55131, Mainz, Germany.
Hugo Ten CateCardiovascular Research Institute Maastricht (CARIM), Maastricht University Medical Center, Maastricht, 6229 HB, The Netherlands.
Philipp S WildClinical Epidemiology and Systems Medicine, Center for Thrombosis and Hemostasis (CTH), University Medical Center of the Johannes Gutenberg University Mainz, 55131, Mainz, Germany. philipp.wild@unimedizin-mainz.de.
Johannes Gutenberg University Mainz · DEUniversity Medical Center of the Johannes Gutenberg University Mainz · DEBayer (Germany) · DEMaastricht University · NLDemocritus University of Thrace · GRDRK Kliniken Berlin · DE

Funding

Marie Curie 813409
6 · The paper itself

Abstract

Animal experiments and early phase human trials suggest that inhibition of factor XIa (FXIa) safely prevents venous thromboembolism (VTE), and specific murine models of sepsis have shown potential efficacy in alleviating cytokine storm. These latter findings support the role of FXI beyond coagulation. Here, we combine targeted proteomics, machine learning and bioinformatics, to discover associations between FXI activity (FXI:C) and the plasma protein profile of patients with VTE. FXI:C was measured with a modified activated partial prothrombin time (APTT) clotting time assay. Proximity extension assay-based protein profiling was performed on plasma collected from subjects from the Genotyping and Molecular Phenotyping of Venous Thromboembolism (GMP-VTE) Project, collected during an acute VTE event (n = 549) and 12-months after (n = 187). Among 444 proteins investigated, N = 21 and N = 66 were associated with FXI:C during the acute VTE event and at 12 months follow-up, respectively. Seven proteins were identified as FXI:C-associated at both time points. These FXI-related proteins were enriched in immune pathways related to causes of thrombo-inflammation, extracellular matrix interaction, lipid metabolism, and apoptosis. The results of this study offer important new avenues for future research into the multiple properties of FXI, which are of high clinical interest given the current development of FXI inhibitors.

Indexed as

Venous ThromboembolismVenous ThrombosisAnimalsApoptosisExtracellular MatrixFactor XIaHumansInflammationLipid MetabolismMiceFactor XIa

Identifiers

PMID35697739
PMCPMC9192691
OpenAlexW4282599402

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.