Evidence map›Paper›PMID 23028599›Full record

ArticlePloS one2012

Retinoic acid signalling is activated in the postischemic heart and may influence remodelling.

Dusan Bilbija, Fred Haugen, Julia Sagave, Anton Baysa, Nasser Bastani, Finn Olav Levy, Allan Sirsjö, Rune Blomhoff, Guro Valen

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

35 citing papers in PubMed, 55 citations in OpenAlex.

  1. Retinoic acid in health and disease.Signal transduction and targeted therapy · 2026
    Review
  2. Review
  3. Article
  4. Retinoic acid signaling and metabolism in heart failure.American journal of physiology. Heart and circulatory physiology · 2025
    Review
  5. Article
  6. Review
  7. Synthetic Retinoids Beyond Cancer Therapy.Annual review of pharmacology and toxicology · 2022
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Role of carotenoids and retinoids during heart development.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2020
    Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. 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

9 authors at 2 institutions in 2 countries.

Dusan BilbijaDepartment of Physiology, University of Oslo, Oslo, Norway. dusan.bilbija@medisin.uio.no
Fred Haugen
Julia Sagave
Anton Baysa
Nasser Bastani
Finn Olav Levy
Allan Sirsjö
Rune Blomhoff
Guro Valen
University of Oslo · NOÖrebro University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAll-trans retinoic acid (atRA), an active derivative of vitamin A, regulates cell differentiation, proliferation and cardiac morphogenesis via transcriptional activation of retinoic acid receptors (RARs) acting on retinoic acid response elements (RARE). We hypothesized that the retinoic acid (RA) signalling pathway is activated in myocardial ischemia and postischemic remodelling. METHODS AND

findingsMyocardial infarction was induced through ligating the left coronary artery in mice. In vivo cardiac activation of the RARs was measured by imaging RARE-luciferase reporter mice, and analysing expression of RAR target genes and proteins by real time RT-PCR and western blot. Endogenous retinoids in postinfarcted hearts were analysed by triple-stage liquid chromatography/tandem mass spectrometry. Cardiomyocytes (CM) and cardiofibroblasts (CF) were isolated from infarcted and sham operated RARE luciferase reporter hearts and monitored for RAR activity and expression of target genes. The effect of atRA on CF proliferation was evaluated by EdU incorporation. Myocardial infarction increased thoracic RAR activity in vivo (p<0.001), which was ascribed to the heart through ex vivo imaging (p = 0.002) with the largest signal 1 week postinfarct. This was accompanied by increased cardiac gene and protein expression of the RAR target genes retinol binding protein 1 (p = 0.01 for RNA, p = 0,006 for protein) and aldehyde dehydrogenase 1A2 (p = 0.04 for RNA, p = 0,014 for protein), while gene expression of cytochrome P450 26B1 was downregulated (p = 0.007). Concomitantly, retinol accumulated in the infarcted zone (p = 0.02). CM and CF isolated from infarcted hearts had higher luminescence than those from sham operated hearts (p = 0.02 and p = 0.008). AtRA inhibited CF proliferation in vitro (p = 0.02).

conclusionThe RA signalling pathway is activated in postischemic hearts and may play a role in regulation of damage and repair during remodelling.

Indexed as

AnimalsHypoxia-Inducible Factor 1MaleMiceMice, Inbred C57BLMustard CompoundsMyocardial InfarctionMyocytes, CardiacPhenylpropionatesReceptors, Retinoic AcidRetinoidsSignal TransductionTretinoin2-amino-3-(4'-N,N-bis(2-chloroethyl)amino)phenylpropionic acid N-oxideHypoxia-Inducible Factor 1Mustard CompoundsPhenylpropionatesReceptors, Retinoic AcidRetinoidsTretinoin

Identifiers

PMID23028599
PMCPMC3460971
OpenAlexW1977742647

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.