Evidence map›Paper›PMID 27730511›Full record

ArticleMolecular neurobiology2017

P2X7 Receptor Signaling Contributes to Sepsis-Associated Brain Dysfunction.

Luiz Eduardo Baggio Savio, Mariana G Juste Andrade, Paola de Andrade Mello, Patrícia Teixeira Santana, Aline Cristina Abreu Moreira-Souza, Janaína Kolling, Aline Longoni, Linda Feldbrügge, Yan Wu, Angela T S Wyse and 2 more

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
4.9field-weighted citation impact, top 5% 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

40 citing papers in PubMed, 64 citations in OpenAlex.

  1. Review
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  5. Targeting P2X Receptors-Current Progress in Sepsis.International journal of inflammation · 2025
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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

12 authors at 3 institutions in 3 countries.

Luiz Eduardo Baggio SavioLaboratory of Immunophysiology, Biophysics Institute Carlos Chagas Filho, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
Mariana G Juste AndradeLaboratory of Immunophysiology, Biophysics Institute Carlos Chagas Filho, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
Paola de Andrade MelloDepartment of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Harvard University, Boston, MA, USA.
Patrícia Teixeira SantanaLaboratory of Immunophysiology, Biophysics Institute Carlos Chagas Filho, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
Aline Cristina Abreu Moreira-SouzaLaboratory of Immunophysiology, Biophysics Institute Carlos Chagas Filho, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
Janaína KollingLaboratory of Neuroprotection and Metabolic Diseases, Department of Biochemistry, Federal University of Rio Grande do Sul, Porto Alegre, RS, Brazil.
Aline LongoniLaboratory of Neuroprotection and Metabolic Diseases, Department of Biochemistry, Federal University of Rio Grande do Sul, Porto Alegre, RS, Brazil.
Linda FeldbrüggeDepartment of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Harvard University, Boston, MA, USA.
Yan WuDepartment of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Harvard University, Boston, MA, USA.
Angela T S WyseLaboratory of Neuroprotection and Metabolic Diseases, Department of Biochemistry, Federal University of Rio Grande do Sul, Porto Alegre, RS, Brazil.
Simon C RobsonDepartment of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Harvard University, Boston, MA, USA.
Robson Coutinho-SilvaLaboratory of Immunophysiology, Biophysics Institute Carlos Chagas Filho, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil. rcsilva@biof.ufrj.br.ORCID http://orcid.org/0000-0002-7318-0204
Universidade Federal do Rio de Janeiro · BRUniversidade Federal do Rio Grande do Sul · BRBeth Israel Deaconess Medical Center · US

Funding

Therapeutic assessment of synthetic heparin sulfates in transplantation modelsP01HL107152 · NHLBI · VIRGINIA COMMONWEALTH UNIVERSITY · PI COOPER, DAVID KC · 2011 to 2017
$15.8M
Initiation of the Sterile Inflammatory Response in Acute PancreatitisK08DK092281 · NIDDK · YALE UNIVERSITY · PI HOQUE, RAFAZ · 2011 to 2015
$774k
NHLBI NIH HHS P01 HL107152NIDDK NIH HHS K08 DK092281
6 · The paper itself

Abstract

Sepsis results in unfettered inflammation, tissue damage, and multiple organ failure. Diffuse brain dysfunction and neurological manifestations secondary to sepsis are termed sepsis-associated encephalopathy (SAE). Extracellular nucleotides, proinflammatory cytokines, and oxidative stress reactions are associated with delirium and brain injury, and might be linked to the pathophysiology of SAE. P2X7 receptor activation by extracellular ATP leads to maturation and release of IL-1β by immune cells, which stimulates the production of oxygen reactive species. Hence, we sought to investigate the role of purinergic signaling by P2X7 in a model of sepsis. We also determined how this process is regulated by the ectonucleotidase CD39, a scavenger of extracellular nucleotides. Wild type (WT), P2X7 receptor (P2X7

Indexed as

AnimalsAntigens, CDApyraseBrainCatalaseCytokinesInflammationMaleMiceMice, KnockoutOxidative StressReceptors, Purinergic P2X7SepsisSignal TransductionSuperoxide DismutaseAntigens, CDApyraseCatalaseCD39 antigenCytokinesReceptors, Purinergic P2X7Superoxide DismutaseBrainCD39Il-1βP2X7 receptorSepsisSTAT3

Identifiers

PMID27730511
OpenAlexW2531093300

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.