Evidence map›Paper›PMID 23543114›Full record

ArticleJournal of neural transmission (Vienna, Austria : 1996)2013

Role of serotonin 5-HT2A receptors in the development of cardiac hypertrophy in response to aortic constriction in mice.

O Lairez, T Cognet, S Schaak, D Calise, C Guilbeau-Frugier, A Parini, J Mialet-Perez

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of neural transmission (Vienna, Austria : 1996), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.8field-weighted citation impact, top 17% 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

24 citing papers in PubMed, 42 citations in OpenAlex.

  1. Review
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  6. Review
  7. Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Cardiac Roles of Serotonin (5-HT) and 5-HT-Receptors in Health and Disease.International journal of molecular sciences · 2023
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Cardiac Outcomes After Perinatal Sertraline Exposure in Mice.Journal of cardiovascular pharmacology · 2017
    Article
  19. Article
  20. 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

7 authors at 1 institution in 1 country.

O LairezINSERM UMR 1048, Institut des Maladies Métaboliques et Cardiovasculaires, BP 84225, 31432, Toulouse Cedex 4, France.
T Cognet
S Schaak
D Calise
C Guilbeau-Frugier
A Parini
J Mialet-Perez
Université Toulouse III - Paul Sabatier · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Serotonin, in addition to its fundamental role as a neurotransmitter, plays a critical role in the cardiovascular system, where it is thought to be involved in the development of cardiac hypertrophy and failure. Indeed, we recently found that mice with deletion of monoamine oxidase A had enhanced levels of blood and cardiac 5-HT, which contributed to exacerbation of hypertrophy in a model of experimental pressure overload. 5-HT2A receptors are expressed in the heart and mediate a hypertrophic response to 5-HT in cardiac cells. However, their role in cardiac remodeling in vivo and the signaling pathways associated are not well understood. In the present study, we evaluated the effect of a selective 5-HT2A receptor antagonist, M100907, on the development of cardiac hypertrophy induced by transverse aortic constriction (TAC). Cardiac 5-HT2A receptor expression was transiently increased after TAC, and was recapitulated in cardiomyocytes, as observed with 5-HT2A in situ labeling by immunohistochemistry. Selective blockade of 5-HT2A receptors prevented the development of cardiac hypertrophy, as measured by echocardiography, cardiomyocyte area and heart weight-to-body weight ratio. Interestingly, activation of calmodulin kinase (CamKII), which is a core mechanism in cardiac hypertrophy, was reduced in cardiac samples from M100907-treated TAC mice compared to vehicle-treated mice. In addition, phosphorylation of histone deacetylase 4 (HDAC4), a downstream partner of CamKII was significantly diminished in M100907-treated TAC mice. Thus, our results show that selective blockade of 5-HT2A receptors has beneficial effect in the development of cardiac hypertrophy through inhibition of the CamKII/HDAC4 pathway.

Indexed as

Age FactorsAnalysis of VarianceAnimalsAortaCalcium-Calmodulin-Dependent Protein Kinase Type 2CardiomegalyConstriction, PathologicDisease Models, AnimalEchocardiographyFluorobenzenesGene Expression RegulationHemodynamicsHistone DeacetylasesMaleMiceMice, Inbred C57BLCalcium-Calmodulin-Dependent Protein Kinase Type 2FluorobenzenesHdac5 protein, mouseHistone DeacetylasesPiperidinesReceptor, Serotonin, 5-HT2ARNA, MessengerSerotonin Antagonistsvolinanserin

Identifiers

PMID23543114
OpenAlexW1967927766

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.