Evidence map›Paper›PMID 30580574›Full record

ReviewArteriosclerosis, thrombosis, and vascular biology2019

Roles of Coagulation Proteases and PARs (Protease-Activated Receptors) in Mouse Models of Inflammatory Diseases.

Jens J Posma, Steven P Grover, Yohei Hisada, A Phillip Owens, Silvio Antoniak, Henri M Spronk, Nigel Mackman

Open access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Arteriosclerosis, thrombosis, and vascular biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
7.2field-weighted citation impact, top 2% 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

56 citing papers in PubMed, 90 citations in OpenAlex.

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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

7 authors at 2 institutions in 2 countries.

Jens J PosmaFrom the Laboratory for Clinical Thrombosis and Hemostasis, Cardiovascular Research Institute Maastricht, Maastricht University Medical Center, The Netherlands (J.J.P., H.M.S.).
Steven P GroverThrombosis and Hemostasis Program, Division of Hematology and Oncology, Department of Medicine, University of North Carolina, Chapel Hill (S.P.G., Y.H., N.M.).
Yohei HisadaThrombosis and Hemostasis Program, Division of Hematology and Oncology, Department of Medicine, University of North Carolina, Chapel Hill (S.P.G., Y.H., N.M.).
A Phillip OwensDivision of Cardiovascular Health and Disease, University of Cincinnati College of Medicine, OH (A.P.O.).
Silvio AntoniakDepartment of Pathology and Laboratory Medicine, University of North Carolina, Chapel Hill (S.A.).
Henri M SpronkFrom the Laboratory for Clinical Thrombosis and Hemostasis, Cardiovascular Research Institute Maastricht, Maastricht University Medical Center, The Netherlands (J.J.P., H.M.S.).
Nigel MackmanThrombosis and Hemostasis Program, Division of Hematology and Oncology, Department of Medicine, University of North Carolina, Chapel Hill (S.P.G., Y.H., N.M.).
University of North Carolina at Chapel Hill · USMaastricht University · NL

Funding

Role of the Thrombin PAR-1 Pathway in Viral InfectionR01HL119523 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI MACKMAN, NIGEL · 2013 to 2020
$3.0M
TISSUE FACTOR GENE REGULATION IN MONOCYTESR01HL048872 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI MACKMAN, NIGEL · 1992 to 2009
$2.9M
Inhibition of PAR2 as therapeutic approach to enhance anti-viral immune responsesR01HL142799 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI ANTONIAK, SILVIO · 2018 to 2022
$1.9M
NHLBI NIH HHS R01 HL048872NHLBI NIH HHS R01 HL119523NHLBI NIH HHS R01 HL142799
6 · The paper itself

Abstract

Activation of the blood coagulation cascade leads to fibrin deposition and platelet activation that are required for hemostasis. However, aberrant activation of coagulation can lead to thrombosis. Thrombi can cause tissue ischemia, and fibrin degradation products and activated platelets can enhance inflammation. In addition, coagulation proteases activate cells by cleavage of PARs (protease-activated receptors), including PAR1 and PAR2. Direct oral anticoagulants have recently been developed to specifically inhibit the coagulation proteases FXa (factor Xa) and thrombin. Administration of these inhibitors to wild-type mice can be used to determine the roles of FXa and thrombin in different inflammatory diseases. These results can be compared with the phenotypes of mice with deficiencies of either Par1 (F2r) or Par2 (F2rl1). However, inhibition of coagulation proteases will have effects beyond reducing PAR signaling, and a deficiency of PARs will abolish signaling from all proteases that activate these receptors. We will summarize studies that examine the roles of coagulation proteases, particularly FXa and thrombin, and PARs in different mouse models of inflammatory disease. Targeting FXa and thrombin or PARs may reduce inflammatory diseases in humans.

Indexed as

Blood CoagulationDisease Models, AnimalAnemia, Sickle CellAnimalsApolipoproteins EAtherosclerosisFactor XaFactor Xa InhibitorsInflammationMiceMyocardial InfarctionReceptors, Proteinase-ActivatedThrombinApolipoproteins EFactor XaFactor Xa InhibitorsReceptors, Proteinase-ActivatedThrombinanticoagulantsblood coagulationinflammationmodels, animalthrombin

Identifiers

PMID30580574
PMCPMC6310042
OpenAlexW2899449506

What OpenQuestion holds

Textmetadata
LicenceTDM
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.