Evidence map›Paper›PMID 22579502›Full record

ReviewDifferentiation; research in biological diversity2012

Atrioventricular valve development: new perspectives on an old theme.

Annemarieke de Vlaming, Kimberly Sauls, Zoltan Hajdu, Richard P Visconti, Agnes Nagy Mehesz, Robert A Levine, Susan A Slaugenhaupt, Albert Hagège, Adrian H Chester, Roger R Markwald and 1 more

Abstract readReview
In one paragraph

Review in Differentiation; research in biological diversity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
–field-weighted citation impact
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

58 citing papers in PubMed.

  1. 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
  2. Mechanisms of mitral valve development and disease.Frontiers in cardiovascular medicine · 2026
    Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Cilia-related diseases.Journal of cellular and molecular medicine · 2023
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Drug discovery of sclerostin inhibitors.Acta pharmaceutica Sinica. B · 2022
    Review
  17. A Systematic Review of Ebstein's Anomaly with Left Ventricular Noncompaction.Journal of cardiovascular development and disease · 2022
    Review
  18. Article
  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

11 authors.

Annemarieke de VlamingDepartment of Regenerative Medicine and Cell Biology, School of Medicine, Cardiovascular Developmental Biology Center, Children's Research Institute, Medical University of South Carolina, Charleston, SC 29425, USA.
Kimberly Sauls
Zoltan Hajdu
Richard P Visconti
Agnes Nagy Mehesz
Robert A Levine
Susan A Slaugenhaupt
Albert Hagège
Adrian H Chester
Roger R Markwald
Russell A Norris

Funding

UBIQUITIN CARBOXYL TERMINAL HYDROLASE L1 (UCH-L1) AND VASCULAR LESION FORMATIONP20RR016434 · NCRR · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI MARKWALD, ROGER R · 2001 to 2011
$24.8M
MUCOPOLYSACCHRIDE METABOLISM IN CARDIAC ANOMALIESR01HL033756 · NHLBI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI MARKWALD, ROGER R · 1985 to 2015
$4.8M
Effect of Mitral Regurgitation on Ischemic LV RemodelingR01HL072265 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI LEVINE, ROBERT A · 2003 to 2013
$3.5M
Improving Mitral Compensation in Ischemic RegurgitationR01HL109506 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI AIKAWA, ELENA, BISCHOFF, JOYCE E. · 2012 to 2015
$3.3M
EXTRAMURAL RESEARCH FACILITIES CONSTRUCTIONC06RR018823 · NCRR · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI RAYMOND, JOHN R · 2003 to 2003
$2.9M
ISCHEMIC MITRAL REGURGITATION: FROM MECHANISM TO THERAPYK24HL067434 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI LEVINE, ROBERT A · 2001 to 2011
$1.6M
NCRR NIH HHS C06 RR018823NCRR NIH HHS C06RR018823NCRR NIH HHS P20 RR016434NCRR NIH HHS P20RR016434-07NCRR NIH HHS P20RR016434-09S1NHLBI NIH HHS K24 HL067434NHLBI NIH HHS R01 HL033756NHLBI NIH HHS R01 HL072265NHLBI NIH HHS R01 HL109506NHLBI NIH HHS R01-HL33756
6 · The paper itself

Abstract

Atrioventricular valve development commences with an EMT event whereby endocardial cells transform into mesenchyme. The molecular events that induce this phenotypic change are well understood and include many growth factors, signaling components, and transcription factors. Besides their clear importance in valve development, the role of these transformed mesenchyme and the function they serve in the developing prevalve leaflets is less understood. Indeed, we know that these cells migrate, but how and why do they migrate? We also know that they undergo a transition to a mature, committed cell, largely defined as an interstitial fibroblast due to their ability to secrete various matrix components including collagen type I. However, we have yet to uncover mechanisms by which the matrix is synthesized, how it is secreted, and how it is organized. As valve disease is largely characterized by altered cell number, cell activation, and matrix disorganization, answering questions of how the valves are built will likely provide us with information of real clinical relevance. Although expression profiling and descriptive or correlative analyses are insightful, to advance the field, we must now move past the simplicity of these assays and ask fundamental, mechanistic based questions aimed at understanding how valves are "built". Herein we review current understandings of atrioventricular valve development and present what is known and what isn't known. In most cases, basic, biological questions and hypotheses that were presented decades ago on valve development still are yet to be answered but likely hold keys to uncovering new discoveries with relevance to both embryonic development and the developmental basis of adult heart valve diseases. Thus, the goal of this review is to remind us of these questions and provide new perspectives on an old theme of valve development.

Indexed as

AnimalsCell DifferentiationCell LineageCell MovementChick EmbryoCollagen Type IEndocardial CushionsEndocardiumEndothelial CellsExtracellular MatrixFibroblastsHeart Defects, CongenitalHeart Valve DiseasesHeart ValvesHumansMesodermCollagen Type I

Identifiers

PMID22579502
PMCPMC3389153

What OpenQuestion holds

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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.