Evidence map›Paper›PMID 36977675›Full record

ArticleNature communications2023

P2X3 receptor antagonism attenuates the progression of heart failure.

Renata M Lataro, Davi J A Moraes, Fabio N Gava, Ana C M Omoto, Carlos A A Silva, Fernanda Brognara, Lais Alflen, Vânia Brazão, Rafaela Pravato Colato, José Clóvis do Prado and 3 more

Open access · goldFull text read
In one paragraph

Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.8field-weighted citation impact, top 6% 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, 25 citations in OpenAlex.

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  15. Purinergic P2XPurinergic signalling · 2024
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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

13 authors at 6 institutions in 3 countries.

Renata M LataroDepartment of Physiological Sciences, Center of Biological Sciences, Federal University of Santa Catarina, Florianópolis, Santa Catarina, Brazil.ORCID 0000-0002-9183-3926
Davi J A MoraesDepartment of Physiology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, Brazil.
Fabio N GavaDepartment of Physiology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, Brazil.
Ana C M OmotoDepartment of Physiology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, Brazil.ORCID 0000-0003-1062-7109
Carlos A A SilvaDepartment of Physiology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, Brazil.
Fernanda BrognaraDepartment of Physiology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, Brazil.ORCID 0000-0002-5042-1319
Lais AlflenDepartment of Physiological Sciences, Center of Biological Sciences, Federal University of Santa Catarina, Florianópolis, Santa Catarina, Brazil.
Vânia BrazãoCollege of Pharmaceutical Sciences of Ribeirão Preto, University of São Paulo, Ribeirão Preto, Brazil.
Rafaela Pravato ColatoCollege of Pharmaceutical Sciences of Ribeirão Preto, University of São Paulo, Ribeirão Preto, Brazil.
José Clóvis do PradoCollege of Pharmaceutical Sciences of Ribeirão Preto, University of São Paulo, Ribeirão Preto, Brazil.
Anthony P FordCuraSen, 2655 Campus Dr #110, San Mateo, CA, 94403, USA.
Helio C SalgadoDepartment of Physiology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, Brazil.ORCID 0000-0001-7351-5740
Julian F R PatonManaaki Manawa-The Centre for Heart Research, Department of Physiology, Faculty of Medical & Health Sciences, University of Auckland, Auckland, New Zealand. j.paton@auckland.ac.nz.
Universidade de São Paulo · BRUniversidade de Ribeirão Preto · BRUniversidade Federal de Santa Catarina · BRCollege of San Mateo · USUniversidade Estadual de Londrina · BRUniversity of Auckland · NZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite advances in the treatment of heart failure, prognosis is poor, mortality high and there remains no cure. Heart failure is associated with reduced cardiac pump function, autonomic dysregulation, systemic inflammation and sleep-disordered breathing; these morbidities are exacerbated by peripheral chemoreceptor dysfunction. We reveal that in heart failure the carotid body generates spontaneous, episodic burst discharges coincident with the onset of disordered breathing in male rats. Purinergic (P2X3) receptors were upregulated two-fold in peripheral chemosensory afferents in heart failure, and when antagonized abolished these episodic discharges, normalized both peripheral chemoreceptor sensitivity and the breathing pattern, reinstated autonomic balance, improved cardiac function, and reduced both inflammation and biomarkers of cardiac failure. Aberrant ATP transmission in the carotid body triggers episodic discharges that via P2X3 receptors play a crucial role in the progression of heart failure and as such offer a distinct therapeutic angle to reverse multiple components of its pathogenesis.

Indexed as

Carotid BodyHeart FailureAnimalsChemoreceptor CellsMaleRatsReceptors, Purinergic P2X3RespirationReceptors, Purinergic P2X3

Identifiers

PMID36977675
PMCPMC10050083
OpenAlexW4361213860

What OpenQuestion holds

Textfull text, public
LicenceCC BY
measurements read114
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.