Evidence map›Paper›PMID 21708977›Full record

ArticleThe Journal of cell biology2011

miR669a and miR669q prevent skeletal muscle differentiation in postnatal cardiac progenitors.

Stefania Crippa, Marco Cassano, Graziella Messina, Daniela Galli, Beatriz G Galvez, Tomaz Curk, Claudia Altomare, Flavio Ronzoni, Jaan Toelen, Rik Gijsbers and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
8.0field-weighted citation impact, top 2% 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

43 citing papers in PubMed, 78 citations in OpenAlex.

  1. Review
  2. The miR-669a-5p/G3BP/HDAC6/AKAP12 Axis Regulates Primary Cilia Length.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  3. Article
  4. Adipocyte · 2022
    Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Non-coding RNAs in Cardiac Regeneration.Frontiers in physiology · 2021
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. MiRNAs as Players in Rhabdomyosarcoma Development.International journal of molecular sciences · 2019
    Review
  19. Review
  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

16 authors at 7 institutions in 5 countries.

Stefania CrippaTranslational Cardiomyology Laboratory, Interdepartmental Stem Cell Institute, Catholic University of Leuven, 3000 Leuven, Belgium.
Marco Cassano
Graziella Messina
Daniela Galli
Beatriz G Galvez
Tomaz Curk
Claudia Altomare
Flavio Ronzoni
Jaan Toelen
Rik Gijsbers
Zeger Debyser
Stefan Janssens
Blaz Zupan
Antonio Zaza
Giulio Cossu
Maurilio Sampaolesi
KU Leuven · BEUniversity of Pavia · ITUniversity of Ljubljana · SIUniversity of Milan · ITUniversity of Milano-Bicocca · ITSpanish National Centre for Cardiovascular Research · ESStem Cell Institute · PA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Postnatal heart stem and progenitor cells are a potential therapeutic tool for cardiomyopathies, but little is known about the mechanisms that control cardiac differentiation. Recent work has highlighted an important role for microribonucleic acids (miRNAs) as regulators of cardiac and skeletal myogenesis. In this paper, we isolated cardiac progenitors from neonatal β-sarcoglycan (Sgcb)-null mouse hearts affected by dilated cardiomyopathy. Unexpectedly, Sgcb-null cardiac progenitors spontaneously differentiated into skeletal muscle fibers both in vitro and when transplanted into regenerating muscles or infarcted hearts. Differentiation potential correlated with the absence of expression of a novel miRNA, miR669q, and with down-regulation of miR669a. Other miRNAs are known to promote myogenesis, but only miR669a and miR669q act upstream of myogenic regulatory factors to prevent myogenesis by directly targeting the MyoD 3' untranslated region. This finding reveals an added level of complexity in the mechanism of the fate choice of mesoderm progenitors and suggests that using endogenous cardiac stem cells therapeutically will require specially tailored procedures for certain genetic diseases.

Indexed as

AnimalsCell DifferentiationDown-RegulationMiceMicroRNAsModels, GeneticMuscle DevelopmentMuscle, SkeletalMyocytes, CardiacRegenerationSarcoglycansStem CellsMicroRNAsSarcoglycans

Identifiers

PMID21708977
PMCPMC3216340
OpenAlexW2032241627

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.