Evidence map›Paper›PMID 33357215›Full record

ReviewCell communication and signaling : CCS2020

Phosphatidylserine inside out: a possible underlying mechanism in the inflammation and coagulation abnormalities of COVID-19.

Gustavo A Argañaraz, Julys da Fonseca Palmeira, Enrique R Argañaraz

Open access · goldAbstract readReview
In one paragraph

Review in Cell communication and signaling : CCS, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
0.8field-weighted citation impact, top 16% 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

30 citing papers in PubMed, 44 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
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  6. Article
  7. Review
  8. Article
  9. Article
  10. A case of hyperhemolysis syndrome in sickle cell disease and concomitant COVID-19.Transfusion and apheresis science : official journal of the World Apheresis Association : official journal of the European Society for Haemapheresis · 2023
    Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. COVID-19 and antiphospholipid antibodies.Best practice & research. Clinical haematology · 2022
    Review
  17. Adamalysins in COVID-19 - Potential mechanisms behind exacerbating the disease.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2022
    Review
  18. Reduced ADAMTS13 Activity in Correlation with Pathophysiology, Severity, and Outcome of COVID-19: A Retrospective Observational Study.International journal of infectious diseases : IJID : official publication of the International Society for Infectious Diseases · 2022
    Observational
  19. Review
  20. Review
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

3 authors at 1 institution in 1 country.

Gustavo A ArgañarazLaboratory of Molecular Neurovirology, Faculty of Health Science, University of Brasília, Brasília, 70910-900, Brazil. gustaad2003@yahoo.com.br.ORCID 0000-0002-1612-2411
Julys da Fonseca PalmeiraLaboratory of Molecular Neurovirology, Faculty of Health Science, University of Brasília, Brasília, 70910-900, Brazil.ORCID 0000-0002-2724-369X
Enrique R ArgañarazLaboratory of Molecular Neurovirology, Faculty of Health Science, University of Brasília, Brasília, 70910-900, Brazil.ORCID 0000-0002-4359-7594
Universidade de Brasília · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The rapid ability of SARS-CoV-2 to spread among humans, along with the clinical complications of coronavirus disease 2019-COVID-19, have represented a significant challenge to the health management systems worldwide. The acute inflammation and coagulation abnormalities appear as the main causes for thousands of deaths worldwide. The intense inflammatory response could be involved with the formation of thrombi. For instance, the presence of uncleaved large multimers of von Willebrand (vWF), due to low ADAMTS13 activity in plasma could be explained by the inhibitory action of pro-inflammatory molecules such as IL-1β and C reactive protein. In addition, the damage to endothelial cells after viral infection and/or activation of endothelium by pro-inflammatory cytokines, such as IL-1β, IL-6, IFN-γ, IL-8, and TNF-α induces platelets and monocyte aggregation in the vascular wall and expression of tissue factor (TF). The TF expression may culminate in the formation of thrombi, and activation of cascade by the extrinsic pathway by association with factor VII. In this scenario, the phosphatidylserine-PtdSer exposure on the outer leaflet of the cell membrane as consequence of viral infection emerges as another possible underlying mechanism to acute immune inflammatory response and activation of coagulation cascade. The PtdSer exposure may be an important mechanism related to ADAM17-mediated ACE2, TNF-α, EGFR and IL-6R shedding, and the activation of TF on the surface of infected endothelial cells. In this review, we address the underlying mechanisms involved in the pathophysiology of inflammation and coagulation abnormalities. Moreover, we introduce key biochemical and pathophysiological concepts that support the possible participation of PtdSer exposure on the outer side of the SARS-CoV-2 infected cells membrane, in the pathophysiology of COVID-19. Video Abstract.

Indexed as

ADAM17 ProteinADAMTS13 ProteinCOVID-19Endothelial CellsHumansInflammationPhosphatidylserinesReceptors, Interleukin-6SARS-CoV-2Thrombosisvon Willebrand FactorADAM17 ProteinADAM17 protein, humanADAMTS13 ProteinIL6R protein, humanPhosphatidylserinesReceptors, Interleukin-6von Willebrand FactorADAM17COVID-19 pathophysiologyDIC-COVID-19Phosphatidylserine

Identifiers

PMID33357215
PMCPMC7765775
OpenAlexW3117798449

What Socratic 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 Socratic graph.