Evidence map›Paper›PMID 21209082›Full record

ArticleThe Journal of biological chemistry2011

Knockdown of cyclin-dependent kinase inhibitors induces cardiomyocyte re-entry in the cell cycle.

Valeria Di Stefano, Mauro Giacca, Maurizio C Capogrossi, Marco Crescenzi, Fabio Martelli

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

61 citing papers in PubMed, 97 citations in OpenAlex.

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  13. Regulation of endogenous cardiomyocyte proliferation: The known unknowns.Journal of molecular and cellular cardiology · 2023
    Review
  14. Btg1 and Btg2 regulate neonatal cardiomyocyte cell cycle arrest.Journal of molecular and cellular cardiology · 2023
    Article
  15. ABRO1 arrests cardiomyocyte proliferation and myocardial repair by suppressing PSPH.Molecular therapy : the journal of the American Society of Gene Therapy · 2023
    Article
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  20. Manipulating Cardiomyocyte Plasticity for Heart Regeneration.Frontiers in cell and developmental biology · 2022
    Review

1 more citing papers are in PubMed but not listed here.

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

5 authors at 4 institutions in 1 country.

Valeria Di StefanoFrom the Molecular Cardiology Laboratory, IRCCS-Policlinico San Donato, San Donato Milanese, 20097 Milan, Italy.
Mauro GiaccaMolecular Medicine Laboratory, International Centre for Genetic Engineering and Biotechnology, 34149 Trieste, Italy.
Maurizio C CapogrossiVascular Pathology Laboratory, Istituto Dermopatico dell'Immacolata-IRCCS, 00167 Rome, Italy, and.
Marco Crescenzithe Department of Environment and Primary Prevention, Istituto Superiore di Sanità, 00161 Rome, Italy.
Fabio MartelliVascular Pathology Laboratory, Istituto Dermopatico dell'Immacolata-IRCCS, 00167 Rome, Italy, and. Electronic address: f.martelli@idi.it.
Istituto Dermopatico dell'Immacolata · ITInternational Centre for Genetic Engineering and Biotechnology · ITIRCCS Policlinico San Donato · ITIstituto Superiore di Sanità · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Proliferation of mammalian cardiomyocytes stops rapidly after birth and injured hearts do not regenerate adequately. High cyclin-dependent kinase inhibitor (CKI) levels have been observed in cardiomyocytes, but their role in maintaining cardiomyocytes in a post-mitotic state is still unknown. In this report, it was investigated whether CKI knockdown by RNA interference induced cardiomyocyte proliferation. We found that triple transfection with p21(Waf1), p27(Kip1), and p57(Kip2) siRNAs induced both neonatal and adult cardiomyocyte to enter S phase and increased the nuclei/cardiomyocyte ratio; furthermore, a subpopulation of cardiomyocytes progressed beyond karyokynesis, as assessed by the detection of mid-body structures and by straight cardiomyocyte counting. Intriguingly, cardiomyocyte proliferation occurred in the absence of overt DNA damage and aberrant mitotic figures. Finally, CKI knockdown and DNA synthesis reactivation correlated with a dramatic change in adult cardiomyocyte morphology that may be a prerequisite for cell division. In conclusion, CKI expression plays an active role in maintaining cardiomyocyte withdrawal from the cell cycle.

Indexed as

AnimalsAnimals, NewbornCell CycleCell LineCyclin-Dependent Kinase Inhibitor ProteinsDNA DamageGene Knockdown TechniquesMiceMuscle ProteinsMyocytes, CardiacRatsRats, WistarRNA InterferenceCyclin-Dependent Kinase Inhibitor ProteinsMuscle Proteins

Identifiers

PMID21209082
PMCPMC3048746
OpenAlexW2082200553

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.