Evidence map›Paper›PMID 27207424›Full record

ReviewThrombosis research2016

The role of EPCR in the pathogenesis of severe malaria.

Laurent O Mosnier, Thomas Lavstsen

Abstract readReview
In one paragraph

Review in Thrombosis research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

18 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Broadly inhibitory antibodies against severe malaria virulence proteins.bioRxiv : the preprint server for biology · 2024
    Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Testing the effect of PAR1 inhibitors onWellcome open research · 2020
    Article
  12. Activated protein C in neuroprotection and malaria.Current opinion in hematology · 2019
    Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Article
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

2 authors at 2 institutions in 2 countries.

Laurent O MosnierDepartment of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, CA. Electronic address: lmosnier@scripps.edu.
Thomas LavstsenCentre for Medical Parasitology, Department of International Health, Immunology & Microbiology, University of Copenhagen and Department of Infectious Diseases, Rigshospitalet, Copenhagen, Denmark.
Rigshospitalet · DKScripps Research Institute · US

Funding

Structure-function of cytoprotective coagulation proteases and their receptorsR01HL104165 · NHLBI · SCRIPPS RESEARCH INSTITUTE, THE · PI MOSNIER, LAURENT OLIVIER · 2011 to 2024
$6.1M
Discovery of novel vascular therapies targeting PfEMP1-mediated cytoadhesion in severe malariaR01HL130678 · NHLBI · SCRIPPS RESEARCH INSTITUTE, THE · PI LAVSTSEN, THOMAS, MOSNIER, LAURENT OLIVIER · 2015 to 2018
$2.0M
NHLBI NIH HHS R01 HL104165NHLBI NIH HHS R01 HL130678
6 · The paper itself

Abstract

Of the five Plasmodium species that infect humans, infection with P. falciparum is the most lethal, causing severe malaria syndromes, that result in over half a million annual deaths. With parasites becoming increasingly resistant to artemisinin there is an urgent need for new preventative and therapeutic options, for which understanding of the mechanisms that cause death and disability in malaria is essential. The recent discoveries that certain variants of P. falciparum erythrocyte membrane protein 1 (PfEMP1) expressed on infected erythrocytes are intimately linked to the precipitation of severe malaria syndromes and that these PfEMP1 variants contain EPCR binding domains provides new opportunities to improve our understanding of the molecular mechanisms responsible for the pathogenesis of severe malaria. EPCR is known for its essential role in the protein C (PC) system and for its ability to support the cytoprotective effects of activated protein C (APC) that result in vascular and tissue protective effects in many organ systems of the body, including the brain, lung, kidney, and liver. Observations that binding of PfEMP1 to EPCR results in an acquired functional PC system deficiency support the new paradigm that EPCR plays a central role in the pathogenesis of severe malaria. Thus, targeting of the PfEMP1-EPCR interaction and restoring the functionality of the PC system may provide new strategies for the development of novel adjuvant therapies for severe malaria.

Indexed as

AnimalsAntigens, CDAntimalarialsDrug DiscoveryEndothelial Protein C ReceptorHost-Parasite InteractionsHumansMalaria, FalciparumMolecular Targeted TherapyPlasmodium falciparumProtein CProtozoan ProteinsReceptors, Cell SurfaceAntigens, CDAntimalarialsEndothelial Protein C Receptorerythrocyte membrane protein 1, Plasmodium falciparumPROCR protein, humanProtein CProtozoan ProteinsReceptors, Cell Surfaceendothelial protein C receptormalariaplasmodium falciparumprotein Cvascular endothelium

Identifiers

PMID27207424
PMCPMC5481197
OpenAlexW2401561733

What OpenQuestion holds

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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.