Evidence map›Paper›PMID 18701451›Full record

ArticleThe Journal of biological chemistry2008

Inflammatory pathways are activated during cardiomyocyte hypertrophy and attenuated by peroxisome proliferator-activated receptors PPARalpha and PPARdelta.

Pascal J H Smeets, Birgit E J Teunissen, Anna Planavila, Heleen de Vogel-van den Bosch, Peter H M Willemsen, Ger J van der Vusse, Marc van Bilsen

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
4.0field-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

46 citing papers in PubMed, 119 citations in OpenAlex.

  1. Review
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  12. Frontiers in physiology · 2021
    Review
  13. Mechanistic insights into cardiovascular protection for omega-3 fatty acids and their bioactive lipid metabolites.European heart journal supplements : journal of the European Society of Cardiology · 2020
    Article
  14. Article
  15. Article
  16. PPARNuclear receptor research · 2018
    Article
  17. Etanercept protects rat cardiomyocytes against hypertrophy by regulating inflammatory cytokines secretion and cell apoptosis.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2017
    Article
  18. Article
  19. Article
  20. New Treatment Strategies for Alcohol-Induced Heart Damage.International journal of molecular sciences · 2016
    Review
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.

Pascal J H SmeetsDepartment of Physiology, Cardiovascular Research Institute Maastricht, Maastricht University, 6200 MD Maastricht, the Netherlands.
Birgit E J Teunissen
Anna Planavila
Heleen de Vogel-van den Bosch
Peter H M Willemsen
Ger J van der Vusse
Marc van Bilsen
Maastricht University · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Accumulating evidence indicates an important role for inflammation in cardiac hypertrophy and failure. Peroxisome proliferator-activated receptors (PPARs) have been reported to attenuate inflammatory signaling pathways and, as such, may interfere with cardiac remodeling. Accordingly, the objectives of the present study were to explore the relationship between cardiomyocyte hypertrophy and inflammation and to investigate whether PPARalpha and PPARdelta are able to inhibit NF-kappaB activation and, consequently, the hypertrophic growth response of neonatal rat cardiomyocytes (NCM). mRNA levels of markers of both hypertrophy and inflammation were increased following treatment with the pro-hypertrophic factor phenylephrine (PE) or the chemokine TNF-alpha. Induction of inflammatory genes was found to be fast (within 2 h after stimulation) and transient, while induction of hypertrophic marker genes was more gradual (peaking at 24-48 h). Inflammatory and hypertrophic pathways appeared to converge on NF-kappaB as both PE and TNF-alpha increased NF-kappaB binding activity as measured by electrophoretic mobility shift assay. Following transient transfection, the p65-induced transcriptional activation of a NF-kappaB reporter construct was significantly blunted after co-transfection of PPARalpha or PPARdelta in the presence of their respective ligands. Finally, adenoviral overexpression of PPARalpha and PPARdelta markedly attenuated cell enlargement and the expression of hypertrophic marker genes in PE-stimulated NCM. The collective findings reveal a close relationship between hypertrophic and inflammatory signaling pathways in the cardiomyocyte. It was shown that both PPARalpha and PPARdelta are able to mitigate cardiomyocyte hypertrophy in vitro by inhibiting NF-kappaB activation.

Indexed as

Gene Expression RegulationInflammationAdenoviridaeAnimalsAnimals, NewbornCardiomegalyModels, BiologicalMyocytes, CardiacNF-kappa BPPAR alphaPPAR deltaRatsRats, Inbred LewSignal TransductionTumor Necrosis Factor-alphaNF-kappa BPPAR alphaPPAR deltaTumor Necrosis Factor-alpha

Identifiers

PMID18701451
PMCPMC2662011
OpenAlexW2025761448

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.