Evidence map›Paper›PMID 26481308›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2016

Cardiac acetylcholine inhibits ventricular remodeling and dysfunction under pathologic conditions.

Ashbeel Roy, Mouhamed Dakroub, Geisa C S V Tezini, Yin Liu, Silvia Guatimosim, Qingping Feng, Helio C Salgado, Vania F Prado, Marco A M Prado, Robert Gros

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

30 citing papers in PubMed, 59 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Production of Acetylcholine by Podocytes and its Protection from Kidney Injury in GN.Journal of the American Society of Nephrology : JASN · 2025
    Article
  5. Review
  6. The Role of Muscarinic Acetylcholine Receptor MInternational journal of molecular sciences · 2024
    Review
  7. Article
  8. Review
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  12. Review
  13. Article
  14. DbhNature communications · 2023
    Article
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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

10 authors at 5 institutions in 2 countries.

Ashbeel Roy*Robarts Research Institute, Department of Physiology and Pharmacology, Department of Medicine, and Department of Anatomy and Cell Biology, The University of Western Ontario, London, Ontario, Canada; Department of Physiology, School of Medicine of Ribeirão Preto, University of São Paulo, Ribeirão Preto, Brazil; and Department of Physiology and Biophysics, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, Brazil.
Mouhamed Dakroub*Robarts Research Institute, Department of Physiology and Pharmacology, Department of Medicine, and Department of Anatomy and Cell Biology, The University of Western Ontario, London, Ontario, Canada; Department of Physiology, School of Medicine of Ribeirão Preto, University of São Paulo, Ribeirão Preto, Brazil; and Department of Physiology and Biophysics, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, Brazil.
Geisa C S V Tezini*Robarts Research Institute, Department of Physiology and Pharmacology, Department of Medicine, and Department of Anatomy and Cell Biology, The University of Western Ontario, London, Ontario, Canada; Department of Physiology, School of Medicine of Ribeirão Preto, University of São Paulo, Ribeirão Preto, Brazil; and Department of Physiology and Biophysics, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, Brazil.
Yin Liu*Robarts Research Institute, Department of Physiology and Pharmacology, Department of Medicine, and Department of Anatomy and Cell Biology, The University of Western Ontario, London, Ontario, Canada; Department of Physiology, School of Medicine of Ribeirão Preto, University of São Paulo, Ribeirão Preto, Brazil; and Department of Physiology and Biophysics, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, Brazil.
Silvia Guatimosim*Robarts Research Institute, Department of Physiology and Pharmacology, Department of Medicine, and Department of Anatomy and Cell Biology, The University of Western Ontario, London, Ontario, Canada; Department of Physiology, School of Medicine of Ribeirão Preto, University of São Paulo, Ribeirão Preto, Brazil; and Department of Physiology and Biophysics, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, Brazil.
Qingping Feng*Robarts Research Institute, Department of Physiology and Pharmacology, Department of Medicine, and Department of Anatomy and Cell Biology, The University of Western Ontario, London, Ontario, Canada; Department of Physiology, School of Medicine of Ribeirão Preto, University of São Paulo, Ribeirão Preto, Brazil; and Department of Physiology and Biophysics, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, Brazil.
Helio C Salgado*Robarts Research Institute, Department of Physiology and Pharmacology, Department of Medicine, and Department of Anatomy and Cell Biology, The University of Western Ontario, London, Ontario, Canada; Department of Physiology, School of Medicine of Ribeirão Preto, University of São Paulo, Ribeirão Preto, Brazil; and Department of Physiology and Biophysics, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, Brazil.
Vania F Prado*Robarts Research Institute, Department of Physiology and Pharmacology, Department of Medicine, and Department of Anatomy and Cell Biology, The University of Western Ontario, London, Ontario, Canada; Department of Physiology, School of Medicine of Ribeirão Preto, University of São Paulo, Ribeirão Preto, Brazil; and Department of Physiology and Biophysics, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, Brazil.
Marco A M Prado*Robarts Research Institute, Department of Physiology and Pharmacology, Department of Medicine, and Department of Anatomy and Cell Biology, The University of Western Ontario, London, Ontario, Canada; Department of Physiology, School of Medicine of Ribeirão Preto, University of São Paulo, Ribeirão Preto, Brazil; and Department of Physiology and Biophysics, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, Brazil mprado@robarts.ca rgros@robarts.ca.
Robert Gros*Robarts Research Institute, Department of Physiology and Pharmacology, Department of Medicine, and Department of Anatomy and Cell Biology, The University of Western Ontario, London, Ontario, Canada; Department of Physiology, School of Medicine of Ribeirão Preto, University of São Paulo, Ribeirão Preto, Brazil; and Department of Physiology and Biophysics, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, Brazil mprado@robarts.ca rgros@robarts.ca.
Western University · CARobarts Clinical Trials · CAUniversidade de Ribeirão Preto · BRUniversidade de São Paulo · BRUniversidade Federal de Minas Gerais · BR

Funding

Decreased Cholinergic Tone and Mitochondrial Dysfunction in HeartR03TW008425 · FIC · UNIVERSITY OF MARYLAND BALTIMORE · PI LEDERER, WILLIAM JONATHAN · 2011 to 2014
$166k
CIHR MOP-82756CIHR MOP-89919FIC NIH HHS R03 TW008425FIC NIH HHS R03TW008425
6 · The paper itself

Abstract

Autonomic dysfunction is a characteristic of cardiac disease and decreased vagal activity is observed in heart failure. Rodent cardiomyocytes produce de novo ACh, which is critical in maintaining cardiac homeostasis. We report that this nonneuronal cholinergic system is also found in human cardiomyocytes, which expressed choline acetyltransferase (ChAT) and the vesicular acetylcholine transporter (VAChT). Furthermore, VAChT expression was increased 3- and 1.5-fold at the mRNA and protein level, respectively, in ventricular tissue from patients with heart failure, suggesting increased ACh secretion in disease. We used mice with genetic deletion of cardiomyocyte-specific VAChT or ChAT and mice overexpressing VAChT to test the functional significance of cholinergic signaling. Mice deficient for VAChT displayed an 8% decrease in fractional shortening and 13% decrease in ejection fraction compared with angiotensin II (Ang II)-treated control animals, suggesting enhanced ventricular dysfunction and pathologic remodeling in response to Ang II. Similar results were observed in ChAT-deficient mice. Conversely, no decline in ventricular function was observed in Ang II-treated VAChT overexpressors. Furthermore, the fibrotic area was significantly greater (P < 0.05) in Ang II-treated VAChT-deficient mice (3.61 ± 0.64%) compared with wild-type animals (2.24 ± 0.11%). In contrast, VAChT overexpressing mice did not display an increase in collagen deposition. Our results provide new insight into cholinergic regulation of cardiac function, suggesting that a compensatory increase in cardiomyocyte VAChT levels may help offset cardiac remodeling in heart failure.

Indexed as

AcetylcholineAnimalsCells, CulturedCholine O-AcetyltransferaseGene Expression Regulation, EnzymologicHeart FailureHumansMaleMiceMice, KnockoutMyocytes, CardiacRNA, MessengerVentricular RemodelingVesicular Acetylcholine Transport ProteinsAcetylcholineCholine O-AcetyltransferaseRNA, MessengerVesicular Acetylcholine Transport Proteinscholine acetyltransferaseheart diseaseheart failurenonneuronal acetylcholineVAChT

Identifiers

PMID26481308
PMCPMC6188225
OpenAlexW2176978240

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.