Evidence map›Paper›PMID 38239348›Full record

ArticleFrontiers in immunology2023

P2Y

Nathália Ferreira Oliveira, Matheus Macedo L V Monteiro, Nathália Santos Mainieri, Augusto Shuiti Tamura, Letícia Massimo Pereira, Leticia Diniz Crepaldi, Robson Coutinho-Silva, Luiz Eduardo Baggio Savio, Claudia Lucia Martins Silva

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

6 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
  2. Review
  3. Endothelial c-IAP2 loss amplifies P2X7 receptor-driven inflammation and worsens schistosomiasis-associated pulmonary hypertension.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  4. Proteasomal-dependent endothelial P2YPurinergic signalling · 2026
    Article
  5. Review
  6. 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

9 authors at 1 institution in 1 country.

Nathália Ferreira OliveiraLaboratório de Farmacologia Bioquímica e Molecular, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
Matheus Macedo L V MonteiroLaboratório de Farmacologia Bioquímica e Molecular, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
Nathália Santos MainieriLaboratório de Farmacologia Bioquímica e Molecular, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
Augusto Shuiti TamuraLaboratório de Imunofisiologia, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
Letícia Massimo PereiraLaboratório de Farmacologia Bioquímica e Molecular, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
Leticia Diniz CrepaldiLaboratório de Imunofisiologia, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
Robson Coutinho-SilvaLaboratório de Imunofisiologia, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
Luiz Eduardo Baggio SavioLaboratório de Imunofisiologia, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
Claudia Lucia Martins SilvaLaboratório de Farmacologia Bioquímica e Molecular, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
Universidade Federal do Rio de Janeiro · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Schistosomiasis is an intravascular infectious disease that impacts over 200 million people globally. In its chronic stage, it leads to mesenteric inflammation with significant involvement of monocytes/macrophages. Endothelial cells lining the vessel lumens play a crucial role, and mount of evidence links this disease to a downregulation of endoprotective cell signaling favoring a primed and proinflammatory endothelial cell phenotype and therefore the loss of immunovascular homeostasis. One hallmark of infectious and inflammatory conditions is the release of nucleotides into the extracellular milieu, which, in turn, act as innate messengers, activating purinergic receptors and triggering cell-to-cell communication. ATP influences the progression of various diseases through P2X and P2Y purinergic receptor subtypes. Among these receptors, P2Y

Indexed as

NF-kappa BSchistosomiasisAnimalsCell AdhesionEndothelial CellsHumansInflammationMiceReceptors, Purinergic P2X7Receptors, Purinergic P2Y2Signal TransductionNF-kappa BP2rx7 protein, mouseP2ry2 protein, mouseReceptors, Purinergic P2X7Receptors, Purinergic P2Y2cell signalingendothelial cellinflammationmesenteric vesselsP2X7 receptorP2Y2 receptorpurinergic signalingschistosomiasis

Identifiers

PMID38239348
PMCPMC10794548
OpenAlexW4390584659

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.