Evidence map›Paper›PMID 23720419›Full record

ReviewAmerican journal of medical genetics. Part C, Seminars in medical genetics2013

Embryonic cardiac chamber maturation: Trabeculation, conduction, and cardiomyocyte proliferation.

Leigh Ann Samsa, Betsy Yang, Jiandong Liu

Open access · greenAbstract readReview
In one paragraph

Review in American journal of medical genetics. Part C, Seminars in medical genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed, 1 pooled it
5.2field-weighted citation impact, top 4% 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

89 citing papers in PubMed, 1 synthesis or guideline pooled it, 171 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Is There a Unified Etiology of Hypoplastic Left Heart Syndrome? Evaluating Genetic, Structural, and Hemodynamic Models of Disease Initiation.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026
    Review
  6. Article
  7. Article
  8. Deletion ofJournal of developmental biology · 2025
    Article
  9. Article
  10. Article
  11. The Mechanics of Building Functional Organs.Cold Spring Harbor perspectives in biology · 2025
    Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. MYH7 in cardiomyopathy and skeletal muscle myopathy.Molecular and cellular biochemistry · 2024
    Review
  19. Article
  20. Human Cardiac Development.Advances in experimental medicine and biology · 2024
    Article

29 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

3 authors at 1 institution in 1 country.

Leigh Ann SamsaUniversity of North Carolina, Chapel Hill, NC, USA.
Betsy Yang
Jiandong Liu
University of North Carolina at Chapel Hill · US

Funding

Pre-doctoral Training Program in Integrative Vascular BiologyT32HL069768 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Christopher P. Mack · 2002 to 2026
$9.7M
Role of hemodynamics and ErbB signaling in cardiac trabeculationR00HL109079 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI LIU, JIANDONG · 2013 to 2015
$742k
Role of hemodynamics and ErbB signaling in cardiac trabeculationK99HL109079 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI LIU, JIANDONG · 2011 to 2012
$178k
NHLBI NIH HHS K99 HL109079NHLBI NIH HHS R00 HL109079NHLBI NIH HHS T32 HL069768
6 · The paper itself

Abstract

Congenital heart diseases are some of the most common human birth defects. Though some congenital heart defects can be surgically corrected, treatment options for other congenital heart diseases are very limited. In many congenital heart diseases, genetic defects lead to impaired embryonic heart development or growth. One of the key development processes in cardiac development is chamber maturation, and alterations in this maturation process can manifest as a variety of congenital defects including non-compaction, systolic dysfunction, diastolic dysfunction, and arrhythmia. During development, to meet the increasing metabolic demands of the developing embryo, the myocardial wall undergoes extensive remodeling characterized by the formation of muscular luminal protrusions called cardiac trabeculae, increased cardiomyocyte mass, and development of the ventricular conduction system. Though the basic morphological and cytological changes involved in early heart development are clear, much remains unknown about the complex biomolecular mechanisms governing chamber maturation. In this review, we highlight evidence suggesting that a wide variety of basic signaling pathways and biomechanical forces are involved in cardiac wall maturation.

Indexed as

Signal TransductionBiomechanical PhenomenaCell ProliferationFetal HeartHeart Conduction SystemHeart Defects, CongenitalHumansMyocytes, CardiacBMPcardiac chamber maturationcardiac trabeculationcardiomyocyte proliferationconductionendothelinEphrinextracellular matrix signalingFGFLeft Ventricular Non-Compaction (LVNC)NeuregulinNotchRetinoic acidSemaphorin

Identifiers

PMID23720419
PMCPMC3723796
OpenAlexW1884080748

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.