Evidence map›Paper›PMID 27323879›Full record

ArticleScientific reports2016

The embryological basis of subclinical hypertrophic cardiomyopathy.

Gabriella Captur, Carolyn Y Ho, Saskia Schlossarek, Janet Kerwin, Mariana Mirabel, Robert Wilson, Stefania Rosmini, Chinwe Obianyo, Patricia Reant, Paul Bassett and 8 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

25 citing papers in PubMed, 43 citations in OpenAlex.

  1. Immature and mature myocardium in the pathophysiology of hypertrophic cardiomyopathy.Journal of molecular and cellular cardiology plus · 2026
    Review
  2. Hypertrophic Cardiomyopathy: Current Perspectives.Reviews in cardiovascular medicine · 2025
    Review
  3. Hypertrophic cardiomyopathy.Nature reviews. Disease primers · 2025
    Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
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  11. Article
  12. Article
  13. Review
  14. Cardiac multi-scale investigation of the right and left ventricleCardiovascular diagnosis and therapy · 2020
    Review
  15. Article
  16. Article
  17. Observational
  18. Article
  19. Coronary arterial vasculature in the pathophysiology of hypertrophic cardiomyopathy.Pflugers Archiv : European journal of physiology · 2019
    Review
  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

18 authors at 8 institutions in 4 countries.

Gabriella CapturUCL Biological Mass Spectrometry Laboratory, Institute of Child Health and Great Ormond Street Hospital, 30 Guilford Street, London, UK.
Carolyn Y HoCardiovascular Division, Brigham and Women's Hospital, Boston MA, USA.
Saskia SchlossarekDepartment of Experimental Pharmacology and Toxicology, Cardiovascular Research Center, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Janet KerwinInstitute of Genetic Medicine, Newcastle University, Newcastle, UK.
Mariana MirabelINSERM U970, Paris Cardiovascular Research Center-PARCC, Paris, France.
Robert WilsonThe Francis Crick Institute Mill Hill Laboratory, The Ridgeway, Mill Hill, London, UK.
Stefania RosminiUCL Institute of Cardiovascular Science, University College London, Gower Street, London, UK.
Chinwe ObianyoUCL Institute of Cardiovascular Science, University College London, Gower Street, London, UK.
Patricia ReantUniversity of Bordeaux, CHU de Bordeaux, CIC1401, Bordeaux, France.
Paul BassettBiostatistics Joint Research Office, University College London, Gower Street, London, UK.
Andrew C CookUCL Institute of Cardiovascular Science, University College London, Gower Street, London, UK.
Susan LindsayInstitute of Genetic Medicine, Newcastle University, Newcastle, UK.
William J McKennaUCL Institute of Cardiovascular Science, University College London, Gower Street, London, UK.
Kevin MillsUCL Biological Mass Spectrometry Laboratory, Institute of Child Health and Great Ormond Street Hospital, 30 Guilford Street, London, UK.
Perry M ElliottUCL Institute of Cardiovascular Science, University College London, Gower Street, London, UK.
Timothy J MohunThe Francis Crick Institute Mill Hill Laboratory, The Ridgeway, Mill Hill, London, UK.
Lucie CarrierDepartment of Experimental Pharmacology and Toxicology, Cardiovascular Research Center, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
James C MoonUCL Institute of Cardiovascular Science, University College London, Gower Street, London, UK.
University College London · GBGreat Ormond Street Hospital · GBNewcastle University · GBThe Francis Crick Institute · GBUniversität Hamburg · DEBrigham and Women's Hospital · USInserm · FRUniversité de Bordeaux · FR

Funding

British Heart Foundation FS/10/40/28260British Heart Foundation FS/12/56/29723Medical Research Council G0700089Medical Research Council MC_PC_15004Medical Research Council U117562103Wellcome TrustWellcome Trust WT100160
6 · The paper itself

Abstract

Hypertrophic cardiomyopathy (HCM) is caused by mutations in sarcomeric proteins, the commonest being MYBPC3 encoding myosin-binding protein C. It is characterised by left ventricular hypertrophy but there is an important pre-hypertrophic phenotype with features including crypts, abnormal mitral leaflets and trabeculae. We investigated these during mouse cardiac development using high-resolution episcopic microscopy. In embryonic hearts from wildtype, homozygous (HO) and heterozygous (HET) Mybpc3-targeted knock-out (KO) mice we show that crypts (one or two) are a normal part of wildtype development but they almost all resolve by birth. By contrast, HO and HET embryos had increased crypt presence, abnormal mitral valve formation and alterations in the compaction process. In scarce normal human embryos, crypts were sometimes present. This study shows that features of the human pre-hypertrophic HCM phenotype occur in the mouse. In an animal model we demonstrate that there is an embryological HCM phenotype. Crypts are a normal part of cardiac development but, along with the mitral valve and trabeculae, their developmental trajectory is altered by the presence of HCM truncating Mybpc3 gene mutation.

Indexed as

AnimalsCardiomyopathy, HypertrophicCarrier ProteinsDisease Models, AnimalGenotypeHeartHumansHypertrophy, Left VentricularMiceMitral ValveMutationMyosin Binding Protein CCarrier ProteinsMyosin Binding Protein C

Identifiers

PMID27323879
PMCPMC4914973
OpenAlexW2470928194

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.