Evidence map›Paper›PMID 22082491›Full record

ArticleCirculation research2012

Fetal cells traffic to injured maternal myocardium and undergo cardiac differentiation.

Rina J Kara, Paola Bolli, Ioannis Karakikes, Iwao Matsunaga, Joseph Tripodi, Omar Tanweer, Perry Altman, Neil S Shachter, Austin Nakano, Vesna Najfeld and 1 more

Erratum issuedAbstract read
In one paragraph

Article in Circulation research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
13.5field-weighted citation impact, top 1% 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

51 citing papers in PubMed, 135 citations in OpenAlex.

  1. Review
  2. Identifying Key Questions and Challenges in Microchimerism Biology.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Presence of fetal microchimerisms in the heart and effect on cardiac repair.Frontiers in cell and developmental biology · 2024
    Article
  8. Article
  9. A Framework for Understanding Maternal Immunity.Immunology and allergy clinics of North America · 2023
    Review
  10. Article
  11. Review
  12. Review
  13. Peripartum cardiomyopathy: a review.Heart failure reviews · 2021
    Review
  14. Regulation of maternal-fetal metabolic communication.Cellular and molecular life sciences : CMLS · 2021
    Review
  15. Review
  16. Review
  17. Review
  18. Article
  19. Review
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 1 institution in 1 country.

Rina J KaraMount Sinai School of Medicine, One Gustave L Levy Place, Box 1030, New York, NY 10029, USA.
Paola Bolli
Ioannis Karakikes
Iwao Matsunaga
Joseph Tripodi
Omar Tanweer
Perry Altman
Neil S Shachter
Austin Nakano
Vesna Najfeld
Hina W Chaudhry
University of California, Los Angeles · US

Funding

The Mechanistic Basis of Cyclin A2-Mediated Cardiac RepairR01HL088255 · NHLBI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI CHAUDHRY, HINA W · 2007 to 2011
$2.2M
NHLBI NIH HHS R01 HL088255NHLBI NIH HHS R01-HL 088255
6 · The paper itself

Abstract

rationaleFetal cells enter the maternal circulation during pregnancy and may persist in maternal tissue for decades as microchimeras.

objectiveBased on clinical observations of peripartum cardiomyopathy patients and the high rate of recovery they experience from heart failure, our objective was to determine whether fetal cells can migrate to the maternal heart and differentiate to cardiac cells. METHODS AND

resultsWe report that fetal cells selectively home to injured maternal hearts and undergo differentiation into diverse cardiac lineages. Using enhanced green fluorescent protein (eGFP)-tagged fetuses, we demonstrate engraftment of multipotent fetal cells in injury zones of maternal hearts. In vivo, eGFP+ fetal cells form endothelial cells, smooth muscle cells, and cardiomyocytes. In vitro, fetal cells isolated from maternal hearts recapitulate these differentiation pathways, additionally forming vascular tubes and beating cardiomyocytes in a fusion-independent manner; ≈40% of fetal cells in the maternal heart express Caudal-related homeobox2 (Cdx2), previously associated with trophoblast stem cells, thought to solely form placenta.

conclusionsFetal maternal stem cell transfer appears to be a critical mechanism in the maternal response to cardiac injury. Furthermore, we have identified Cdx2 cells as a novel cell type for potential use in cardiovascular regenerative therapy.

Indexed as

AnimalsCDX2 Transcription FactorCell DifferentiationCell MovementCells, CulturedEndothelium, VascularFemaleFetal Stem CellsGreen Fluorescent ProteinsHomeodomain ProteinsIn Vitro TechniquesMaleMaternal-Fetal ExchangeMiceMice, Inbred StrainsMice, TransgenicCdx2 protein, mouseCDX2 Transcription FactorGreen Fluorescent ProteinsHomeodomain ProteinsTranscription Factors

Identifiers

PMID22082491
PMCPMC3365532
OpenAlexW2138835306

What OpenQuestion holds

Textmetadata
LicenceTDM
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.