Evidence map›Paper›PMID 34935057›Full record

ReviewInternational journal of molecular medicine2022

Host cell entry mediators implicated in the cellular tropism of SARS‑CoV‑2, the pathophysiology of COVID‑19 and the identification of microRNAs that can modulate the expression of these mediators (Review).

Periklis Katopodis, Harpal S Randeva, Demetrios A Spandidos, Sayeh Saravi, Ioannis Kyrou, Emmanouil Karteris

Open access · bronzeAbstract readReview
In one paragraph

Review in International journal of molecular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 13% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.

  1. Pooled it
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  3. Article
  4. A survey of SARS-CoV-2 tropism.Infectious diseases & immunity · 2025
    Review
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  11. Review
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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

6 authors at 3 institutions in 2 countries.

Periklis Katopodis *Biosciences, College of Health, Medicine and Life Sciences, Brunel University London, Uxbridge UB8 3PH, UK.
Harpal S RandevaWarwickshire Institute for The Study of Diabetes, Endocrinology and Metabolism (WISDEM), University Hospitals Coventry and Warwickshire NHS Trust, Coventry CV2 2DX, UK.
Demetrios A SpandidosLaboratory of Clinical Virology, Medical School, University of Crete, 71409 Heraklion, Greece.
Sayeh SaraviBiosciences, College of Health, Medicine and Life Sciences, Brunel University London, Uxbridge UB8 3PH, UK.
Ioannis KyrouWarwickshire Institute for The Study of Diabetes, Endocrinology and Metabolism (WISDEM), University Hospitals Coventry and Warwickshire NHS Trust, Coventry CV2 2DX, UK.
Emmanouil Karteris *Biosciences, College of Health, Medicine and Life Sciences, Brunel University London, Uxbridge UB8 3PH, UK.
Brunel University of London · GBUniversity Hospitals Coventry and Warwickshire NHS Trust · GBUniversity of Crete · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The pathophysiology of coronavirus disease 2019 (COVID‑19) is mainly dependent on the underlying mechanisms that mediate the entry of severe acute respiratory syndrome coronavirus 2 (SARS‑CoV‑2) into the host cells of the various human tissues/organs. Recent studies have indicated a higher order of complexity of the mechanisms of infectivity, given that there is a wide‑repertoire of possible cell entry mediators that appear to co‑localise in a cell‑ and tissue‑specific manner. The present study provides an overview of the 'canonical' SARS‑CoV‑2 mediators, namely angiotensin converting enzyme 2, transmembrane protease serine 2 and 4, and neuropilin‑1, expanding on the involvement of novel candidates, including glucose‑regulated protein 78, basigin, kidney injury molecule‑1, metabotropic glutamate receptor subtype 2, ADAM metallopeptidase domain 17 (also termed tumour necrosis factor‑α convertase) and Toll‑like receptor 4. Furthermore, emerging data indicate that changes in microRNA (miRNA/miR) expression levels in patients with COVID‑19 are suggestive of further complexity in the regulation of these viral mediators. An

Indexed as

Virus InternalizationAngiotensin-Converting Enzyme 2COVID-19Endoplasmic Reticulum Chaperone BiPGene Expression RegulationHost-Pathogen InteractionsHumansMembrane ProteinsMicroRNAsNeuropilin-1Receptors, VirusSARS-CoV-2Serine EndopeptidasesSpike Glycoprotein, CoronavirusToll-Like Receptor 4Viral TropismAngiotensin-Converting Enzyme 2Endoplasmic Reticulum Chaperone BiPMembrane ProteinsMicroRNAsNeuropilin-1Receptors, VirusSerine EndopeptidasesSpike Glycoprotein, CoronavirusTMPRSS2 protein, humanTMPRSS4 protein, humanToll-Like Receptor 4ACE2ADAM17COVID‑19GRP78miRNAsNPR1SARS‑CoV2TLR4TMPRSS2TMPRSS4

Identifiers

PMID34935057
PMCPMC8722767
OpenAlexW4200436346

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.