Evidence map›Paper›PMID 28673898›Full record

ArticleJournal of the American Heart Association2017

Platelet-Derived Factor V Is a Critical Mediator of Arterial Thrombosis.

Meiping Ren, Rong Li, Ni Chen, Ningbo Pang, Yongjie Li, Xin Deng, Liqun Wang, Mao Luo, Yan Liu, Haiyan Hao and 3 more

Open access · goldAbstract read
In one paragraph

Article in Journal of the American Heart Association, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 2 pooled it
1.6field-weighted citation impact, top 16% 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

13 citing papers in PubMed, 2 syntheses or guidelines pooled it, 17 citations in OpenAlex.

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  12. Microfluidic endothelium-on-a-chip development, from in vivo to in vitro experimental models.Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologie · 2020
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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

13 authors at 2 institutions in 2 countries.

Meiping RenDrug Discovery Research Center, Southwest Medical University, Luzhou, Sichuan, China.
Rong LiDrug Discovery Research Center, Southwest Medical University, Luzhou, Sichuan, China.
Ni ChenDrug Discovery Research Center, Southwest Medical University, Luzhou, Sichuan, China.
Ningbo PangDrug Discovery Research Center, Southwest Medical University, Luzhou, Sichuan, China.
Yongjie LiDrug Discovery Research Center, Southwest Medical University, Luzhou, Sichuan, China.
Xin DengDrug Discovery Research Center, Southwest Medical University, Luzhou, Sichuan, China.
Liqun WangDrug Discovery Research Center, Southwest Medical University, Luzhou, Sichuan, China.
Mao LuoDrug Discovery Research Center, Southwest Medical University, Luzhou, Sichuan, China.
Yan LiuDrug Discovery Research Center, Southwest Medical University, Luzhou, Sichuan, China.
Haiyan HaoDrug Discovery Research Center, Southwest Medical University, Luzhou, Sichuan, China.
Yong LiuDrug Discovery Research Center, Southwest Medical University, Luzhou, Sichuan, China.
Hongmin SunDepartment of Medicine, University of Missouri School of Medicine, Columbia, MO.
Jianbo WuDrug Discovery Research Center, Southwest Medical University, Luzhou, Sichuan, China wuji@missouri.edu.
Southwest Medical University · CNUniversity of Missouri · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCoagulation factor V (FV) plays a key role in hemostasis, is present in plasma and platelets, and has both pro- and anticoagulant properties; however, the contribution of platelet-derived FV to arterial thrombosis remains undetermined. METHODS AND

resultsUsing transgenic mice with various levels of FV gene expression that was restricted to the plasma or platelets, the roles of platelet FV were evaluated in the regulation of arterial thrombosis and platelet activation. Mice with higher levels of platelet FV exhibited faster thrombotic occlusion of the carotid artery after injury compared with mice with lower platelet FV levels. Infusion of platelets with higher levels of FV into transgenic mice with undetectable levels of platelet FV reduced the time to carotid artery occlusion. In contrast, infusion of purified recombinant plasma FV into mice with undetectable platelet FV levels failed to reduce the carotid occlusion times following injury. Evaluation of isolated platelets revealed that platelet-derived FV was critical for the regulation of platelet activation. These effects were associated with an increased level of expression of P-selectin and increased cGMP in platelets.

conclusionsWe established that platelet-derived FV is a critical mediator of arterial thrombosis that involves platelet activation.

Indexed as

Blood CoagulationPlatelet ActivationAnimalsBlood PlateletsCarotid Artery DiseasesCyclic GMPDisease Models, AnimalFactor VGenetic Predisposition to DiseaseInfusions, IntravenousMaleMice, KnockoutPhenotypeRecombinant ProteinsSelenoprotein PThrombosisCyclic GMPFactor VRecombinant ProteinsSelenoprotein PTransforming Growth Factor betaarterialcoagulationfactor Vplateletthrombosis

Identifiers

PMID28673898
PMCPMC5586322
OpenAlexW2729077587

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.