Evidence map›Paper›PMID 33302737›Full record

ReviewExperimental biology and medicine (Maywood, N.J.)2021

Protease-activated receptor 1 as a potential therapeutic target for COVID-19.

Emanuel S Rovai, Tomaz Alves, Marinella Holzhausen

Open access · hybridAbstract readReview
In one paragraph

Review in Experimental biology and medicine (Maywood, N.J.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
0.5field-weighted citation impact, top 21% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. International journal of molecular sciences · 2023
    Article
  8. Microvascular Thrombosis as a Critical Factor in Severe COVID-19.International journal of molecular sciences · 2023
    Article
  9. Review
  10. Sars-Cov2 Induced Biochemical Mechanisms in Liver Damage and Intestinal Lesions.Indian journal of clinical biochemistry : IJCB · 2022
    Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. 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 2 institutions in 1 country.

Emanuel S RovaiDepartment of Dentistry, University of Taubate, Taubate 12010-490, Brazil.
Tomaz AlvesDivision of Periodontics, Department of Stomatology, School of Dentistry, University of São Paulo, São Paulo 05508-000, Brazil.
Marinella HolzhausenDivision of Periodontics, Department of Stomatology, School of Dentistry, University of São Paulo, São Paulo 05508-000, Brazil.ORCID 0000-0001-9413-5253
Universidade de São Paulo · BRUniversidade de Taubaté · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute respiratory disease caused by a novel coronavirus (SARS-CoV-2) has spread all over the world, since its discovery in 2019, Wuhan, China. This disease is called COVID-19 and already killed over 1 million people worldwide. The clinical symptoms include fever, dry cough, dyspnea, headache, dizziness, generalized weakness, vomiting, and diarrhea. Unfortunately, so far, there is no validated vaccine, and its management consists mainly of supportive care. Venous thrombosis and pulmonary embolism are highly prevalent in patients suffering from severe COVID-19. In fact, a prothrombotic state seems to be present in most fatal cases of the disease. SARS-CoV-2 leads to the production of proinflammatory cytokines, causing immune-mediated tissue damage, disruption of the endothelial barrier, and uncontrolled thrombogenesis. Thrombin is the key regulator of coagulation and fibrin formation. In severe COVID-19, a dysfunctional of physiological anticoagulant mechanisms leads to a progressive increase of thrombin activity, which is associated with acute respiratory distress syndrome development and a poor prognosis. Protease-activated receptor type 1 (PAR1) is the main thrombin receptor and may represent an essential link between coagulation and inflammation in the pathophysiology of COVID-19. In this review, we discuss the potential role of PAR1 inhibition and regulation in COVID-19 treatment.

Indexed as

AnticoagulantsBlood CoagulationBlood Coagulation FactorsCOVID-19COVID-19 Drug TreatmentDisseminated Intravascular CoagulationHumansPlatelet Aggregation InhibitorsPulmonary EmbolismReceptor, PAR-1Receptors, Cell SurfaceSARS-CoV-2ThrombinVenous Thrombosisactivated protein C receptorAnticoagulantsBlood Coagulation FactorsPlatelet Aggregation InhibitorsReceptor, PAR-1Receptors, Cell SurfaceThrombinanticoagulationcoagulopathycoronavirusCOVID-19Protease-activated receptor 1proteases

Identifiers

PMID33302737
PMCPMC7746952
OpenAlexW3113267780

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.