Evidence map›Paper›PMID 32751741›Full record

ArticleDiagnostics (Basel, Switzerland)2020

COVID-19-Related Coagulopathy-Is Transferrin a Missing Link?

Katie-May McLaughlin, Marco Bechtel, Denisa Bojkova, Christian Münch, Sandra Ciesek, Mark N Wass, Martin Michaelis, Jindrich Cinatl

Open access · goldAbstract read
In one paragraph

Article in Diagnostics (Basel, Switzerland), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
0.8field-weighted citation impact, top 15% 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

21 citing papers in PubMed, 39 citations in OpenAlex.

  1. The research progress of ferroptosis in acute lung injury.Biochemistry and biophysics reports · 2026
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  18. Recent Progress of Ferroptosis in Lung Diseases.Frontiers in cell and developmental biology · 2021
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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

8 authors at 2 institutions in 2 countries.

Katie-May McLaughlinSchool of Biosciences, University of Kent, Canterbury CT2 7NJ, UK.
Marco BechtelInstitute for Medical Virology, University Hospital, Goethe University, 60596 Frankfurt am Main, Germany.
Denisa BojkovaInstitute for Medical Virology, University Hospital, Goethe University, 60596 Frankfurt am Main, Germany.
Christian MünchInstitute of Biochemistry II, Faculty of Medicine, Goethe University, 60590 Frankfurt am Main, Germany.
Sandra CiesekInstitute for Medical Virology, University Hospital, Goethe University, 60596 Frankfurt am Main, Germany.ORCID 0000-0002-1802-7565
Mark N WassSchool of Biosciences, University of Kent, Canterbury CT2 7NJ, UK.ORCID 0000-0001-5428-6479
Martin MichaelisSchool of Biosciences, University of Kent, Canterbury CT2 7NJ, UK.ORCID 0000-0002-5710-5888
Jindrich CinatlInstitute for Medical Virology, University Hospital, Goethe University, 60596 Frankfurt am Main, Germany.
Goethe University Frankfurt · DEUniversity of Kent · GB

Funding

Frankfurter Stiftung für krebskranke Kinder n/aHilfe für krebskranke Kinder Frankfurt e.V. n/a
6 · The paper itself

Abstract

SARS-CoV-2 is the causative agent of COVID-19. Severe COVID-19 disease has been associated with disseminated intravascular coagulation and thrombosis, but the mechanisms underlying COVID-19-related coagulopathy remain unknown. The risk of severe COVID-19 disease is higher in males than in females and increases with age. To identify gene products that may contribute to COVID-19-related coagulopathy, we analyzed the expression of genes associated with the Gene Ontology (GO) term "blood coagulation" in the Genotype-Tissue Expression (GTEx) database and identified four procoagulants, whose expression is higher in males and increases with age (ADAMTS13, F11, HGFAC, KLKB1), and two anticoagulants, whose expression is higher in females and decreases with age (C1QTNF1, SERPINA5). However, the expression of none of these genes was regulated in a proteomics dataset of SARS-CoV-2-infected cells and none of the proteins have been identified as a binding partner of SARS-CoV-2 proteins. Hence, they may rather generally predispose individuals to thrombosis without directly contributing to COVID-19-related coagulopathy. In contrast, the expression of the procoagulant transferrin (not associated to the GO term "blood coagulation") was higher in males, increased with age, and was upregulated upon SARS-CoV-2 infection. Hence, transferrin warrants further examination in ongoing clinic-pathological investigations.

Indexed as

coagulationcoagulopathyCOVID-19SARS-CoV-2thrombosistransferrin

Identifiers

PMID32751741
PMCPMC7459734
OpenAlexW3046315871

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.