Evidence map›Paper›PMID 28680883›Full record

ReviewBioMed research international2017

The Interaction of Selectins and PSGL-1 as a Key Component in Thrombus Formation and Cancer Progression.

János Kappelmayer, Béla Nagy

Open access · hybridAbstract readReview
In one paragraph

Review in BioMed research international, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed, 2 pooled it
3.9field-weighted citation impact, top 6% 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

60 citing papers in PubMed, 2 syntheses or guidelines pooled it, 105 citations in OpenAlex.

  1. Pooled it
  2. The Role of P-Selectin in COVID-19 Coagulopathy: An Updated Review.International journal of molecular sciences · 2021
    Pooled it
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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

2 authors at 1 institution in 1 country.

János KappelmayerDepartment of Laboratory Medicine, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.ORCID 0000-0002-3599-4717
Béla NagyDepartment of Laboratory Medicine, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
University of Debrecen · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cellular interaction is inevitable in the pathomechanism of human disease. Formation of heterotypic cellular aggregates, between distinct cells of hematopoietic and nonhematopoietic origin, may be involved in events leading to inflammation and the complex process of cancer progression. Among adhesion receptors, the family of selectins with their ligands have been considered as one of the major contributors to cell-cell interactions. Consequently, the inhibition of the interplay between selectins and their ligands may have potential therapeutic benefits. In this review, we focus on the current evidence on the selectins as crucial modulators of inflammatory, thrombotic, and malignant disorders. Knowing that there is promiscuity in selectin binding, we outline the importance of a key protein that serves as a ligand for all selectins. This dimeric mucin, the P-selectin glycoprotein ligand 1 (PSGL-1), has emerged as a major player in inflammation, thrombus, and cancer development. We discuss the interaction of PSGL-1 with various selectins in physiological and pathological processes with particular emphasis on mechanisms that lead to severe disease.

Indexed as

AnimalsHumansMembrane GlycoproteinsNeoplasm ProteinsNeoplasmsSelectinsThrombosisMembrane GlycoproteinsNeoplasm ProteinsP-selectin ligand proteinSelectins

Identifiers

PMID28680883
PMCPMC5478826
OpenAlexW2617383260

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.