Evidence map›Paper›PMID 27472922›Full record

ArticleStem cell research & therapy2016

Bmi1 (+) cardiac progenitor cells contribute to myocardial repair following acute injury.

Iñigo Valiente-Alandi, Carmen Albo-Castellanos, Diego Herrero, Iria Sanchez, Antonio Bernad

Open access · goldAbstract read
In one paragraph

Article in Stem cell research & therapy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

31 citing papers in PubMed, 43 citations in OpenAlex.

  1. Review
  2. Heart-derived endogenous stem cells.Molecular biology reports · 2025
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  7. Development of aInternational journal of molecular sciences · 2024
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  9. The Vascular Niche for Adult Cardiac Progenitor Cells.Antioxidants (Basel, Switzerland) · 2022
    Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. Review
  16. Cardiac Progenitor Cells.Advances in experimental medicine and biology · 2021
    Review
  17. Article
  18. Review
  19. Article
  20. 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

5 authors at 2 institutions in 1 country.

Iñigo Valiente-AlandiCardiovascular Development and Repair Department, Spanish National Cardiovascular Research Center (CNIC), Madrid, Spain.
Carmen Albo-CastellanosCardiovascular Development and Repair Department, Spanish National Cardiovascular Research Center (CNIC), Madrid, Spain.
Diego HerreroCardiovascular Development and Repair Department, Spanish National Cardiovascular Research Center (CNIC), Madrid, Spain.
Iria SanchezUnidad de Medicina Comparada, Cardiovascular Development and Repair Department, Spanish National Cardiovascular Research Center (CNIC), Madrid, Spain.
Antonio BernadCardiovascular Development and Repair Department, Spanish National Cardiovascular Research Center (CNIC), Madrid, Spain. abernad@cnb.csic.es.
Spanish National Centre for Cardiovascular Research · ESCentro Nacional de Biotecnología · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe inability of the adult mammalian heart to replace cells lost after severe cardiac injury compromises organ function. Although the heart is one of the least regenerative organs in the body, evidence accumulated in recent decades indicates a certain degree of renewal after injury. We have evaluated the role of cardiac Bmi1 (+) progenitor cells (Bmi1-CPC) following acute myocardial infarction (AMI).

methodsBmi1 (Cre/+);Rosa26 (YFP/+) (Bmi1-YFP) mice were used for lineage tracing strategy. After tamoxifen (TM) induction, yellow fluorescent protein (YFP) is expressed under the control of Rosa26 regulatory sequences in Bmi1 (+) cells. YFP(+) cells were tracked following myocardial infarction. Additionally, whole transcriptome analysis of isolated YFP(+) cells was performed in unchallenged hearts and after myocardial infarction.

resultsDeep-sequencing analysis of Bmi1-CPC from unchallenged hearts suggests that this population expresses high levels of pluripotency markers. Conversely, transcriptome evaluation of Bmi1-CPC following AMI shows a rich representation of genes related to cell proliferation, movement, and cell cycle. Lineage-tracing studies after cardiac infarction show that the progeny of Bmi1-expressing cells contribute to de novo cardiomyocytes (CM) (13.8 ± 5 % new YFP(+) CM compared to 4.7 ± 0.9 % in age-paired non-infarcted hearts). However, apical resection of TM-induced day 1 Bmi1-YFP pups indicated a very minor contribution of Bmi1-derived cells to de novo CM.

conclusionsCardiac Bmi1 progenitor cells respond to cardiac injury, contributing to the generation of de novo CM in the adult mouse heart.

Indexed as

TranscriptomeAnimalsBacterial ProteinsCell DifferentiationCell ProliferationCell TrackingDisease Models, AnimalFemaleGene Expression RegulationHumansLuminescent ProteinsMaleMiceMice, TransgenicMyocardial InfarctionMyocardiumBacterial ProteinsBmi1 protein, mouseGt(ROSA)26Sor non-coding RNA, mouseLuminescent ProteinsPolycomb Repressive Complex 1Proto-Oncogene ProteinsRNA, UntranslatedTamoxifenyellow fluorescent protein, BacteriaBmi1Cardiac progenitor cellsMyocardial infarctionStem cells

Identifiers

PMID27472922
PMCPMC4967328
OpenAlexW2483061171

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.