Evidence map›Paper›PMID 32925166›Full record

ReviewThe Journal of clinical investigation2020

Complement and coagulation: key triggers of COVID-19-induced multiorgan pathology.

Berhane Ghebrehiwet, Ellinor I Peerschke

Open access · bronzeAbstract readReview
In one paragraph

Review in The Journal of clinical investigation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Post-COVID-19 Syndrome Mechanisms, Prevention and Management.International journal of preventive medicine · 2023
    Review
  10. Article
  11. Clinical challenges of SARS-CoV-2 variants (Review).Experimental and therapeutic medicine · 2022
    Review
  12. Article
  13. Review
  14. Review
  15. Review
  16. Review
  17. Article
  18. Article
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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 2 institutions in 1 country.

Berhane GhebrehiwetDepartment of Medicine, Stony Brook University, Stony Brook, New York, USA.
Ellinor I PeerschkeDepartment of Laboratory Medicine, Memorial Sloan Kettering Cancer Center, New York, New York, USA.
Memorial Sloan Kettering Cancer Center · USStony Brook University · US

Funding

gC1q-R/p33: structure function and role on inflammation.R01AI060866 · NIAID · STATE UNIVERSITY NEW YORK STONY BROOK · PI GHEBREHIWET, BERHANE · 2006 to 2009
$1.2M
The role of C1q in regulation of monocyte to dendritic cell transitionR01AI084178 · NIAID · STATE UNIVERSITY NEW YORK STONY BROOK · PI GHEBREHIWET, BERHANE · 2009 to 2010
$602k
gC1qR as a therapeutic target for angioedema.R56AI122376 · NIAID · STATE UNIVERSITY NEW YORK STONY BROOK · PI GHEBREHIWET, BERHANE · 2018 to 2018
$477k
NIAID NIH HHS R01 AI060866NIAID NIH HHS R01 AI084178NIAID NIH HHS R56 AI122376
6 · The paper itself

Abstract

In a stunningly short period of time, the unexpected coronavirus disease 2019 (COVID-19) pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has turned the unprepared world topsy-turvy. Although the rapidity with which the virus struck was indeed overwhelming, scientists throughout the world have been up to the task of deciphering the mechanisms by which SARS-CoV-2 induces the multisystem and multiorgan inflammatory responses that, collectively, contribute to the high mortality rate in affected individuals. In this issue of the JCI, Skendros and Mitsios et al. is one such team who report that the complement system plays a substantial role in creating the hyperinflammation and thrombotic microangiopathy that appear to contribute to the severity of COVID-19. In support of the hypothesis that the complement system along with neutrophils and platelets contributes to COVID-19, the authors present empirical evidence showing that treatment with the complement inhibitor compstatin Cp40 inhibited the expression of tissue factor in neutrophils. These results confirm that the complement axis plays a critical role and suggest that targeted therapy using complement inhibitors is a potential therapeutic option to treat COVID-19-induced inflammation.

Indexed as

Coronavirus InfectionsPandemicsPneumonia, ViralThrombotic MicroangiopathiesBetacoronavirusBlood PlateletsComplement ActivationCOVID-19HumansInflammationNeutrophilsPeptides, CyclicSARS-CoV-2Severity of Illness IndexThromboplastincompstatinPeptides, CyclicThromboplastin

Identifiers

PMID32925166
PMCPMC7598033
OpenAlexW3084456691

What OpenQuestion holds

Textmetadata
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.