Evidence map›Paper›PMID 22057716›Full record

ArticleBasic research in cardiology2011

Left ventricular remodeling in swine after myocardial infarction: a transcriptional genomics approach.

Diederik W D Kuster, Daphne Merkus, Andreas Kremer, Wilfred F J van Ijcken, Vincent J de Beer, Adrie J M Verhoeven, Dirk J Duncker

Open access · hybridAbstract read
In one paragraph

Article in Basic research in cardiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 19% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.

  1. Pooled it
  2. The microtubule signature in cardiac disease: etiology, disease stage, and age dependency.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2023
    Article
  3. Corticosteroid Receptors in Cardiac Health and Disease.Advances in experimental medicine and biology · 2022
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. UM206, a selective Frizzled antagonist, attenuates adverse remodeling after myocardial infarction in swine.Laboratory investigation; a journal of technical methods and pathology · 2016
    Article
  12. Article
  13. Transcriptional profiling of HMGB1-induced myocardial repair identifies a key role for Notch signaling.Molecular therapy : the journal of the American Society of Gene Therapy · 2013
    Article
  14. Article
  15. Article
  16. 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 2 institutions in 1 country.

Diederik W D KusterDivision of Experimental Cardiology, Thoraxcenter, Erasmus MC, University Medical Center Rotterdam, P. O. Box 2040, 3000 CA Rotterdam, The Netherlands.
Daphne Merkus
Andreas Kremer
Wilfred F J van Ijcken
Vincent J de Beer
Adrie J M Verhoeven
Dirk J Duncker
Erasmus MC · NLErasmus University Rotterdam · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite the apparent appropriateness of left ventricular (LV) remodeling following myocardial infarction (MI), it poses an independent risk factor for development of heart failure. There is a paucity of studies into the molecular mechanisms of LV remodeling in large animal species. We took an unbiased molecular approach to identify candidate transcription factors (TFs) mediating the genetic reprogramming involved in post-MI LV remodeling in swine. Left ventricular tissue was collected from remote, non-infarcted myocardium, 3 weeks after MI-induction or sham-surgery. Microarray analysis identified 285 upregulated and 278 downregulated genes (FDR < 0.05). Of these differentially expressed genes, the promoter regions of the human homologs were searched for common TF binding sites (TFBS). Eighteen TFBS were overrepresented >two-fold (p < 0.01) in upregulated and 13 in downregulated genes. Left ventricular nuclear protein extracts were assayed for DNA-binding activity by protein/DNA array. Out of 345 DNA probes, 30 showed signal intensity changes >two-fold. Five TFs were identified in both TFBS and protein/DNA array analyses, which showed matching changes for COUP-TFII and glucocorticoid receptor (GR) only. Treatment of swine with the GR antagonist mifepristone after MI reduced the post-MI increase in LV mass, but LV dilation remained unaffected. Thus, using an unbiased approach to study post-MI LV remodeling in a physiologically relevant large animal model, we identified COUP-TFII and GR as potential key mediators of post-MI remodeling.

Indexed as

Gene Expression ProfilingAnimalsCOUP Transcription Factor IIDisease Models, AnimalEchocardiographyFemaleGenomicsMaleMyocardial InfarctionOligonucleotide Array Sequence AnalysisReceptors, GlucocorticoidSwineTranscription FactorsVentricular RemodelingCOUP Transcription Factor IIReceptors, GlucocorticoidTranscription Factors

Identifiers

PMID22057716
PMCPMC3228945
OpenAlexW2112528840

What OpenQuestion holds

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LicenceCC BY-NC
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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.