Evidence map›Paper›PMID 32932519›Full record

ArticleBlood2021

Xenotropic and polytropic retrovirus receptor 1 regulates procoagulant platelet polyphosphate.

Reiner K Mailer, Mikel Allende, Marco Heestermans, Michaela Schweizer, Carsten Deppermann, Maike Frye, Giordano Pula, Jacob Odeberg, Mathias Gelderblom, Stefan Rose-John and 10 more

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 9% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. The contact system in liver injury.Seminars in immunopathology · 2021
    Review
  19. Proteomics: A Tool to Study Platelet Function.International journal of molecular sciences · 2021
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

20 authors at 8 institutions in 7 countries.

Reiner K MailerInstitute of Clinical Chemistry and Laboratory Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Mikel AllendeInstitute of Clinical Chemistry and Laboratory Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Marco HeestermansInstitute of Clinical Chemistry and Laboratory Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Michaela SchweizerElectron Microscopy Unit, Center for Molecular Neurobiology (ZMNH), University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Carsten DeppermannInstitute of Clinical Chemistry and Laboratory Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Maike FryeInstitute of Clinical Chemistry and Laboratory Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Giordano PulaInstitute of Clinical Chemistry and Laboratory Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Jacob OdebergK. G. Jebsen Thrombosis Research and Expertise Centre (TREC), Department of Clinical Medicine, The Arctic University of Norway, Tromsø, Norway.
Mathias GelderblomDepartment of Neurology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Stefan Rose-JohnInstitute of Biochemistry, University of Kiel, Kiel, Germany.
Albert SickmannLeibniz-Institut für Analytische Wissenschaften (ISAS) eV, Dortmund, Germany.
Stefan BlankenbergDepartment of General and Interventional Cardiology, University Heart Center, Hamburg, Germany.
Tobias B HuberDepartment of Medicine III and.
Christian KubischInstitute of Human Genetics, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Coen MaasDepartment of Clinical Chemistry and Hematology, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands.
Stepan GambaryanSechenov Institute of Evolutionary Physiology and Biochemistry, Russian Academy of Sciences, St Petersburg, Russia.
Dmitri FirsovDepartment of Pharmacology and Toxicology, University of Lausanne, Lausanne, Switzerland.
Evi X StavrouDepartment of Medicine, Louis Stokes Cleveland Veterans Affairs (VA) Medical Center, Cleveland, OH; and.
Lynn M ButlerInstitute of Clinical Chemistry and Laboratory Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Thomas RennéInstitute of Clinical Chemistry and Laboratory Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Universität Hamburg · DEChristian-Albrechts-Universität zu Kiel · DEInstitute of Evolutionary Physiology and Biochemistry · RULeibniz Institute for Analytical Sciences - ISAS · DELouis Stokes Cleveland VA Medical Center · USUiT The Arctic University of Norway · NOUniversity of Lausanne · CHUtrecht University · NL

Funding

Treatment of Deep Vein Thrombosis via Targeted Inhibition of the FXII-uPAR-pAkt2 Axis in NeutrophilsI01BX003851 · VA · LOUIS STOKES CLEVELAND VA MEDICAL CENTER · PI Evi X. Stavrou · 2020 to 2026
–
BLRD VA I01 BX003851
6 · The paper itself

Abstract

Polyphosphate is a procoagulant inorganic polymer of linear-linked orthophosphate residues. Multiple investigations have established the importance of platelet polyphosphate in blood coagulation; however, the mechanistic details of polyphosphate homeostasis in mammalian species remain largely undefined. In this study, xenotropic and polytropic retrovirus receptor 1 (XPR1) regulated polyphosphate in platelets and was implicated in thrombosis in vivo. We used bioinformatic analyses of omics data to identify XPR1 as a major phosphate transporter in platelets. XPR1 messenger RNA and protein expression inversely correlated with intracellular polyphosphate content and release. Pharmacological interference with XPR1 activity increased polyphosphate stores, led to enhanced platelet-driven coagulation, and amplified thrombus formation under flow via the polyphosphate/factor XII pathway. Conditional gene deletion of Xpr1 in platelets resulted in polyphosphate accumulation, accelerated arterial thrombosis, and augmented activated platelet-driven pulmonary embolism without increasing bleeding in mice. These data identify platelet XPR1 as an integral regulator of platelet polyphosphate metabolism and reveal a fundamental role for phosphate homeostasis in thrombosis.

Indexed as

AnimalsBiological TransportBlood CoagulationBlood PlateletsFactor XIIFemaleMaleMicePolyphosphatesReceptors, G-Protein-CoupledReceptors, VirusThrombosisXenotropic and Polytropic Retrovirus ReceptorFactor XIIPolyphosphatesReceptors, G-Protein-CoupledReceptors, VirusXenotropic and Polytropic Retrovirus ReceptorXPR1 protein, humanXpr1 protein, mouse

Identifiers

PMID32932519
PMCPMC7955403
OpenAlexW3087283112

What OpenQuestion holds

Textmetadata
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.