Evidence map›Paper›PMID 34537482›Full record

ReviewInternational immunopharmacology2021

Targeting purinergic receptors to suppress the cytokine storm induced by SARS-CoV-2 infection in pulmonary tissue.

Júlia Leão Batista Simões, Helena Fornari Basso, Greicy Cristine Kosvoski, Jullye Gavioli, Filomena Marafon, Charles Elias Assmann, Fabiano Barbosa Carvalho, Margarete Dulce Bagatini

Open access · greenAbstract readReview
In one paragraph

Review in International immunopharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
2.8field-weighted citation impact, top 11% 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

8 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Irreversible Antagonists for the Adenosine AMolecules (Basel, Switzerland) · 2022
    Article
  8. 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

8 authors at 4 institutions in 1 country.

Júlia Leão Batista SimõesMedical School, Federal University of Fronteira Sul, Chapecó, SC, Brazil.
Helena Fornari BassoNursing School, Federal University of Fronteira Sul, Chapecó, SC, Brazil.
Greicy Cristine KosvoskiNursing School, Federal University of Fronteira Sul, Chapecó, SC, Brazil.
Jullye GavioliMedical School, Federal University of Fronteira Sul, Chapecó, SC, Brazil.
Filomena MarafonPostgraduate Program in Biochemistry, Federal University of Santa Catarina, Florianópolis, SC, Brazil.
Charles Elias AssmannPostgraduate Program in Biological Sciences: Toxicological Biochemistry, Federal University of Santa Maria, Santa Maria, RS, Brazil.
Fabiano Barbosa CarvalhoFederal University of Health Sciences of Porto Alegre, Porto Alegre, RS, Brazil.
Margarete Dulce BagatiniGraduate Program in Medical Sciences, Federal University of Fronteira Sul, Chapecó, SC, Brazil. Electronic address: margaretebagatini@yahoo.com.br.
Universidade Federal da Fronteira Sul · BRUniversidade Federal de Ciências da Saúde de Porto Alegre · BRUniversidade Federal de Santa Catarina · BRUniversidade Federal de Santa Maria · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The etiological agent of coronavirus disease (COVID-19) is the new member of the Coronaviridae family, a severe acute respiratory syndrome coronavirus 2 virus (SARS-CoV-2), responsible for the pandemic that is plaguing the world. The single-stranded RNA virus is capable of infecting the respiratory tract, by binding the spike (S) protein on its viral surface to receptors for the angiotensin II-converting enzyme (ACE2), highly expressed in the pulmonary tissue, enabling the interaction of the virus with alveolar epithelial cells promoting endocytosis and replication of viral material. The infection triggers the activation of the immune system, increased purinergic signaling, and the release of cytokines as a defense mechanism, but the response can become exaggerated and prompt the so-called "cytokine storm", developing cases such as severe acute respiratory syndrome (SARS). This is characterized by fever, cough, and difficulty breathing, which can progress to pneumonia, failure of different organs and death. Thus, the present review aims to compile and correlate the mechanisms involved between the immune and purinergic systems with COVID-19, since the modulation of purinergic receptors, such as A2A, A2B, and P2X7 expressed by immune cells, seems to be effective as a promising therapy, to reduce the severity of the disease, as well as aid in the treatment of acute lung diseases and other cases of generalized inflammation.

Indexed as

SARS-CoV-2Adenosine TriphosphateCOVID-19Cytokine Release SyndromeHumansInflammationReceptors, PurinergicSeverity of Illness IndexSignal TransductionAdenosine TriphosphateReceptors, PurinergicAdenosineATPCoronavirusP2X7Purinergic signalingTherapy

Identifiers

PMID34537482
PMCPMC8435372
OpenAlexW3199835103

What Socratic 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 Socratic graph.