Evidence map›Paper›PMID 30899802›Full record

ArticleBiochemistry and biophysics reports2019

Neuronal NO synthase mediates plenylephrine induced cardiomyocyte hypertrophy through facilitation of NFAT-dependent transcriptional activity.

Xavier Loyer, Caroline Dubroca, Maxime Branchereau, Graziellia Griffith, Luis Garcia, Christophe Heymes

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

Article in Biochemistry and biophysics reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.1field-weighted citation impact, top 49% 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

0 citing papers in PubMed, 1 citations in OpenAlex.

No citing paper in PubMed yet.

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

6 authors at 3 institutions in 1 country.

Xavier LoyerINSERM UMR-S 970, Paris Cardiovascular Research Center, France.
Caroline DubrocaINSERM U1048 -Institut des Maladies Métaboliques et Cardiovacsulaires (I2MC), Toulouse, France.
Maxime BranchereauINSERM U1048 -Institut des Maladies Métaboliques et Cardiovacsulaires (I2MC), Toulouse, France.
Graziellia GriffithUniversité de Versailles St-Quentin, INSERM U1179, Montigny-le-Bretonneux, France.
Luis GarciaUniversité de Versailles St-Quentin, INSERM U1179, Montigny-le-Bretonneux, France.
Christophe HeymesINSERM U1048 -Institut des Maladies Métaboliques et Cardiovacsulaires (I2MC), Toulouse, France.
Inserm · FRDélégation Paris 5 · FRUniversité Toulouse III - Paul Sabatier · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuronal nitric oxide synthase (NOS1) has been consistently shown to be the predominant isoform of NOS and/or NOS-derived NO that may be involved in the myocardial remodeling including cardiac hypertrophy. However, the direct functional contribution of NOS1 in this process remains to be elucidated. Therefore, in the present study, we attempted to use silent RNA and adenovirus mediated silencing or overexpression to investigate the role of NOS1 and the associated molecular signaling mechanisms during OKphenylephrine (PE)-induced cardiac hypertrophy growth in neonatal rat ventricular cardiomyocytes (NRVMs). We found that the expression of NOS1 was enhanced in PE-induced hypertrophic cardiomyocytes. Moreover, LVNIO treatment, a selective NOS1 inhibitor, significantly decreased PE-induced NRVMs hypertrophy and [

Indexed as

AdenovirusCardiomyocyte hypertrophyGene silencingNeuronal NO synthaseNFAT

Identifiers

PMID30899802
PMCPMC6412025
OpenAlexW2922182426

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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.