Evidence map›Paper›PMID 28576718›Full record

ArticleJournal of molecular and cellular cardiology2017

Effect of altered haemodynamics on the developing mitral valve in chick embryonic heart.

Kar Lai Pang, Matthew Parnall, Siobhan Loughna

Abstract read
In one paragraph

Article in Journal of molecular and cellular cardiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Science advances · 2024
    Article
  6. Review
  7. Article
  8. Mechanosensitive Pathways in Heart Development: Findings from Chick Embryo Studies.Journal of cardiovascular development and disease · 2021
    Review
  9. Review
  10. Biomechanical Cues Direct Valvulogenesis.Journal of cardiovascular development and disease · 2020
    Review
  11. Article
  12. Development and evolution of the metazoan heart.Developmental dynamics : an official publication of the American Association of Anatomists · 2019
    Review
  13. Review
  14. Article
  15. Hemodynamics in Cardiac Development.Journal of cardiovascular development and disease · 2018
    Article
  16. Review
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.

Kar Lai PangSchool of Life Sciences, Medical School, University of Nottingham, Nottingham NG7 2UH, UK.
Matthew ParnallSchool of Life Sciences, Medical School, University of Nottingham, Nottingham NG7 2UH, UK.
Siobhan LoughnaSchool of Life Sciences, Medical School, University of Nottingham, Nottingham NG7 2UH, UK. Electronic address: Siobhan.loughna@nottingham.ac.uk.

Funding

British Heart Foundation FS/12/44/29619
6 · The paper itself

Abstract

Intracardiac haemodynamics is crucial for normal cardiogenesis, with recent evidence showing valvulogenesis is haemodynamically dependent and inextricably linked with shear stress. Although valve anomalies have been associated with genetic mutations, often the cause is unknown. However, altered haemodynamics have been suggested as a pathogenic contributor to bicuspid aortic valve disease. Conversely, how abnormal haemodynamics impacts mitral valve development is still poorly understood. In order to analyse altered blood flow, the outflow tract of the chick heart was constricted using a ligature to increase cardiac pressure overload. Outflow tract-banding was performed at HH21, with harvesting at crucial valve development stages (HH26, HH29 and HH35). Although normal valve morphology was found in HH26 outflow tract banded hearts, smaller and dysmorphic mitral valve primordia were seen upon altered haemodynamics in histological and stereological analysis at HH29 and HH35. A decrease in apoptosis, and aberrant expression of a shear stress responsive gene and extracellular matrix markers in the endocardial cushions were seen in the chick HH29 outflow tract banded hearts. In addition, dysregulation of extracellular matrix (ECM) proteins fibrillin-2, type III collagen and tenascin were further demonstrated in more mature primordial mitral valve leaflets at HH35, with a concomitant decrease of ECM cross-linking enzyme, transglutaminase-2. These data provide compelling evidence that normal haemodynamics are a prerequisite for normal mitral valve morphogenesis, and abnormal blood flow could be a contributing factor in mitral valve defects, with differentiation as a possible underlying mechanism.

Indexed as

HemodynamicsAnimalsBiomarkersChick EmbryoExtracellular MatrixGene Expression ProfilingHeartHeart Defects, CongenitalMitral ValveOrganogenesisT-Box Domain ProteinsBiomarkersT-Box Domain ProteinsCardiac valve developmentHaemodynamicsMitral valveOutflow tract bandingValve defectValvulogenesis

Identifiers

PMID28576718
PMCPMC5529288

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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.