Evidence map›Paper›PMID 35719336›Full record

ReviewFrontiers in cellular and infection microbiology2022

Pathophysiology of COVID-19: Critical Role of Hemostasis.

Sonia Aparecida de Andrade, Daniel Alexandre de Souza, Amarylis Lins Torres, Cristiane Ferreira Graça de Lima, Matteo Celano Ebram, Rosa Maria Gaudioso Celano, Mirta Schattner, Ana Marisa Chudzinski-Tavassi

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cellular and infection microbiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 7% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Microvascular Thrombosis as a Critical Factor in Severe COVID-19.International journal of molecular sciences · 2023
    Article
  11. Platelets in COVID-19 disease: friend, foe, or both?Pharmacological reports : PR · 2022
    Review
  12. Article
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 3 institutions in 2 countries.

Sonia Aparecida de AndradeBiopharmaceuticals Laboratory, Instituto Butantan, São Paulo, Brazil.
Daniel Alexandre de SouzaBiopharmaceuticals Laboratory, Instituto Butantan, São Paulo, Brazil.
Amarylis Lins TorresBiopharmaceuticals Laboratory, Instituto Butantan, São Paulo, Brazil.
Cristiane Ferreira Graça de LimaBiopharmaceuticals Laboratory, Instituto Butantan, São Paulo, Brazil.
Matteo Celano EbramBiopharmaceuticals Laboratory, Instituto Butantan, São Paulo, Brazil.
Rosa Maria Gaudioso CelanoUniversity of Taubaté (UNITAU), Taubaté, Brazil.
Mirta SchattnerLaboratory of Experimental Thrombosis. Instituto de Medicina Experimental - CONICET -Academia Nacional de Medicina, Buenos Aires, Argentina.
Ana Marisa Chudzinski-TavassiCenter of Excellence in New Target Discovery (CENTD), Instituto Butantan, São Paulo, Brazil.
Instituto Butantan · BRConsejo Nacional de Investigaciones Científicas y Técnicas · ARUniversidade de Taubaté · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The COVID-19 pandemic, caused by SARS-CoV-2, had its first cases identified in late 2019 and was considered a clinical pandemic in March 2020. In March 2022, more than 500 million people were infected and 6,2 million died as a result of this disease, increasingly associated with changes in human hemostasis, such as hypercoagulation. Numerous factors contribute to the hypercoagulable state, and endothelial dysfunction is the main one, since the activation of these cells can strongly activate platelets and the coagulation system. In addition, there is a dysregulation of the renin-angiotensin system due to the SARS-CoV-2 takeover of the angiotensin converting enzyme 2, resulting in a strong immune response that could further damage the endothelium. Thrombus formation in the pulmonary microvasculature structure in patients with COVID-19 is an important factor to determine the severity of the clinical picture and the outcome of this disease. This review describes the hemostatic changes that occur in SARS-CoV-2 infection, to further improve our understanding of pathogenic mechanisms and the interaction between endothelium dysfunction, kallikrein-kinins, renin angiotensin, and the Coagulation/fibrinolysis systems as underlying COVID-19 effectors. This knowledge is crucial for the development of new effective therapeutic approaches, attenuating the severity of SARS-CoV-2's infection and to reduce the deaths.

Indexed as

COVID-19HemostasisHumansPandemicsPeptidyl-Dipeptidase ARenin-Angiotensin SystemSARS-CoV-2Peptidyl-Dipeptidase AcoagulopathyCOVID-19hemostasisSARS-CoV-2thrombus

Identifiers

PMID35719336
PMCPMC9205169
OpenAlexW4281953742

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.