Evidence map›Paper›PMID 24751578›Full record

ArticlePloS one2014

An analysis of the global expression of microRNAs in an experimental model of physiological left ventricular hypertrophy.

Nidiane C Martinelli, Carolina R Cohen, Kátia G Santos, Mauro A Castro, Andréia Biolo, Luzia Frick, Daiane Silvello, Amanda Lopes, Stéfanie Schneider, Michael E Andrades and 3 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

28 citing papers in PubMed, 60 citations in OpenAlex.

  1. Plasma levels of microRNA in chronic kidney disease: patterns in acute and chronic exercise.American journal of physiology. Heart and circulatory physiology · 2015
    Trial
  2. Review
  3. MicroRNAs regulating signaling pathways in cardiac fibrosis: potential role of the exercise training.American journal of physiology. Heart and circulatory physiology · 2024
    Review
  4. Review
  5. Exosomal microRNAs in diabetic heart disease.Cardiovascular diabetology · 2022
    Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Noncoding RNAs in Cardiac Hypertrophy.Journal of cardiovascular translational research · 2018
    Review
  12. Review
  13. The Role of MicroRNAs in the Cardiac Response to Exercise.Cold Spring Harbor perspectives in medicine · 2017
    Review
  14. MicroRNA profiling identifies miR-7-5p and miR-26b-5p as differentially expressed in hypertensive patients with left ventricular hypertrophy.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2017
    Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. MicroRNA Regulatory Network Revealing the Mechanism of Inflammation in Atrial Fibrillation.Medical science monitor : international medical journal of experimental and clinical research · 2015
    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

13 authors at 2 institutions in 1 country.

Nidiane C MartinelliExperimental and Molecular Cardiovascular Laboratory and the Heart Failure and Cardiac Transplant Unit from the Cardiology Division at Hospital de Clínicas de Porto Alegre, Porto Alegre, RS, Brazil; Post-Graduate Program in Cardiology and Cardiovascular Science, Porto Alegre, RS, Brazil; Post-Graduate Program in Genetics and Molecular Biology at the Federal University of Rio Grande do Sul, Porto Alegre, RS, Brazil.
Carolina R CohenExperimental and Molecular Cardiovascular Laboratory and the Heart Failure and Cardiac Transplant Unit from the Cardiology Division at Hospital de Clínicas de Porto Alegre, Porto Alegre, RS, Brazil; Post-Graduate Program in Cardiology and Cardiovascular Science, Porto Alegre, RS, Brazil; Post-Graduate Program in Genetics and Molecular Biology at the Federal University of Rio Grande do Sul, Porto Alegre, RS, Brazil.
Kátia G SantosExperimental and Molecular Cardiovascular Laboratory and the Heart Failure and Cardiac Transplant Unit from the Cardiology Division at Hospital de Clínicas de Porto Alegre, Porto Alegre, RS, Brazil; Post-Graduate Program in Cardiology and Cardiovascular Science, Porto Alegre, RS, Brazil.
Mauro A CastroExperimental and Molecular Cardiovascular Laboratory and the Heart Failure and Cardiac Transplant Unit from the Cardiology Division at Hospital de Clínicas de Porto Alegre, Porto Alegre, RS, Brazil.
Andréia BioloExperimental and Molecular Cardiovascular Laboratory and the Heart Failure and Cardiac Transplant Unit from the Cardiology Division at Hospital de Clínicas de Porto Alegre, Porto Alegre, RS, Brazil; Post-Graduate Program in Cardiology and Cardiovascular Science, Porto Alegre, RS, Brazil.
Luzia FrickExperimental and Molecular Cardiovascular Laboratory and the Heart Failure and Cardiac Transplant Unit from the Cardiology Division at Hospital de Clínicas de Porto Alegre, Porto Alegre, RS, Brazil.
Daiane SilvelloExperimental and Molecular Cardiovascular Laboratory and the Heart Failure and Cardiac Transplant Unit from the Cardiology Division at Hospital de Clínicas de Porto Alegre, Porto Alegre, RS, Brazil; Post-Graduate Program in Cardiology and Cardiovascular Science, Porto Alegre, RS, Brazil.
Amanda LopesExperimental and Molecular Cardiovascular Laboratory and the Heart Failure and Cardiac Transplant Unit from the Cardiology Division at Hospital de Clínicas de Porto Alegre, Porto Alegre, RS, Brazil.
Stéfanie SchneiderExperimental and Molecular Cardiovascular Laboratory and the Heart Failure and Cardiac Transplant Unit from the Cardiology Division at Hospital de Clínicas de Porto Alegre, Porto Alegre, RS, Brazil; Post-Graduate Program in Cardiology and Cardiovascular Science, Porto Alegre, RS, Brazil.
Michael E AndradesExperimental and Molecular Cardiovascular Laboratory and the Heart Failure and Cardiac Transplant Unit from the Cardiology Division at Hospital de Clínicas de Porto Alegre, Porto Alegre, RS, Brazil; Post-Graduate Program in Cardiology and Cardiovascular Science, Porto Alegre, RS, Brazil.
Nadine ClausellExperimental and Molecular Cardiovascular Laboratory and the Heart Failure and Cardiac Transplant Unit from the Cardiology Division at Hospital de Clínicas de Porto Alegre, Porto Alegre, RS, Brazil; Post-Graduate Program in Cardiology and Cardiovascular Science, Porto Alegre, RS, Brazil.
Ursula MattePost-Graduate Program in Cardiology and Cardiovascular Science, Porto Alegre, RS, Brazil; Post-Graduate Program in Genetics and Molecular Biology at the Federal University of Rio Grande do Sul, Porto Alegre, RS, Brazil.
Luis E RohdeExperimental and Molecular Cardiovascular Laboratory and the Heart Failure and Cardiac Transplant Unit from the Cardiology Division at Hospital de Clínicas de Porto Alegre, Porto Alegre, RS, Brazil; Post-Graduate Program in Cardiology and Cardiovascular Science, Porto Alegre, RS, Brazil.
Hospital de Clínicas de Porto Alegre · BRUniversidade Federal do Rio Grande do Sul · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMicroRNAs (miRs) are a class of small non-coding RNAs that regulate gene expression. Studies of transgenic mouse models have indicated that deregulation of a single miR can induce pathological cardiac hypertrophy and cardiac failure. The roles of miRs in the genesis of physiological left ventricular hypertrophy (LVH), however, are not well understood.

objectiveTo evaluate the global miR expression in an experimental model of exercise-induced LVH.

methodsMale Balb/c mice were divided into sedentary (SED) and exercise (EXE) groups. Voluntary exercise was performed on an odometer-monitored metal wheels for 35 days. Various tests were performed after 7 and 35 days of training, including a transthoracic echocardiography, a maximal exercise test, a miR microarray (miRBase v.16) and qRT-PCR analysis.

resultsThe ratio between the left ventricular weight and body weight was increased by 7% in the EXE group at day 7 (p<0.01) and by 11% at day 35 of training (p<0.001). After 7 days of training, the microarray identified 35 miRs that were differentially expressed between the two groups: 20 were up-regulated and 15 were down-regulated in the EXE group compared with the SED group (p = 0.01). At day 35 of training, 25 miRs were differentially expressed: 15 were up-regulated and 10 were decreased in the EXE animals compared with the SED animals (p<0.01). The qRT-PCR analysis demonstrated an increase in miR-150 levels after 35 days and a decrease in miR-26b, miR-27a and miR-143 after 7 days of voluntary exercise.

conclusionsWe have identified new miRs that can modulate physiological cardiac hypertrophy, particularly miR-26b, -150, -27a and -143. Our data also indicate that previously established regulatory gene pathways involved in pathological LVH are not changed in physiological LVH.

Indexed as

Gene Expression RegulationAnimalsBody WeightDisease Models, AnimalHypertrophy, Left VentricularMaleMice, Inbred BALB CMicroRNAsOligonucleotide Array Sequence AnalysisPhysical Conditioning, AnimalReal-Time Polymerase Chain ReactionReproducibility of ResultsSignal TransductionUltrasonographyMicroRNAs

Identifiers

PMID24751578
PMCPMC3994002
OpenAlexW2056578184

What OpenQuestion holds

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LicenceCC BY
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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.