Evidence map›Paper›PMID 21862559›Full record

ArticleDevelopment (Cambridge, England)2011

Knockdown of embryonic myosin heavy chain reveals an essential role in the morphology and function of the developing heart.

Catrin Sian Rutland, Luis Polo-Parada, Elisabeth Ehler, Aziza Alibhai, Aaran Thorpe, Suganthi Suren, Richard D Emes, Bhakti Patel, Siobhan Loughna

Open access · bronzeAbstract read
In one paragraph

Article in Development (Cambridge, England), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.1field-weighted citation impact, top 11% 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

19 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Modulation of mechanosensitive genes during embryonic aortic arch development.Developmental dynamics : an official publication of the American Association of Anatomists · 2025
    Article
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  6. Defective sarcomere organization and reduced larval locomotion and fish survival in slow muscle heavy chain 1 (smyhc1) mutants.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
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  9. Review
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  13. Persistent Noggin arrests cardiomyocyte morphogenesis and results in early in utero lethality.Developmental dynamics : an official publication of the American Association of Anatomists · 2015
    Article
  14. Article
  15. Article
  16. Article
  17. Heavy and light roles: myosin in the morphogenesis of the heart.Cellular and molecular life sciences : CMLS · 2013
    Review
  18. Article
  19. 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

9 authors at 2 institutions in 1 country.

Catrin Sian RutlandSchool of Biomedical Sciences, University of Nottingham, Queens Medical Centre, Derby Road, Nottingham, NG7 2UH, UK.
Luis Polo-Parada
Elisabeth Ehler
Aziza Alibhai
Aaran Thorpe
Suganthi Suren
Richard D Emes
Bhakti Patel
Siobhan Loughna
Queen's Medical Centre · GBUniversity of Nottingham · GB

Funding

British Heart Foundation PG/06/021/20345British Heart Foundation RG/07/010/23676Medical Research Council G0400153Medical Research Council G0700089Medical Research Council G9900837Wellcome TrustWellcome Trust 082557
6 · The paper itself

Abstract

The expression and function of embryonic myosin heavy chain (eMYH) has not been investigated within the early developing heart. This is despite the knowledge that other structural proteins, such as alpha and beta myosin heavy chains and cardiac alpha actin, play crucial roles in atrial septal development and cardiac function. Most cases of atrial septal defects and cardiomyopathy are not associated with a known causative gene, suggesting that further analysis into candidate genes is required. Expression studies localised eMYH in the developing chick heart. eMYH knockdown was achieved using morpholinos in a temporal manner and functional studies were carried out using electrical and calcium signalling methodologies. Knockdown in the early embryo led to abnormal atrial septal development and heart enlargement. Intriguingly, action potentials of the eMYH knockdown hearts were abnormal in comparison with the alpha and beta myosin heavy chain knockdowns and controls. Although myofibrillogenesis appeared normal, in knockdown hearts the tissue integrity was affected owing to apparent focal points of myocyte loss and an increase in cell death. An expression profile of human skeletal myosin heavy chain genes suggests that human myosin heavy chain 3 is the functional homologue of the chick eMYH gene. These data provide compelling evidence that eMYH plays a crucial role in important processes in the early developing heart and, hence, is a candidate causative gene for atrial septal defects and cardiomyopathy.

Indexed as

AnimalsAnimals, Genetically ModifiedCardiomyopathy, DilatedChick EmbryoEmbryo, MammalianGene Knockdown TechniquesHeartHeart Defects, CongenitalHumansMiceMorphogenesisMyocardiumMyosin Heavy ChainsOrganogenesisSurvivalValidation Studies as TopicMyosin Heavy Chains

Identifiers

PMID21862559
PMCPMC3160091
OpenAlexW2106727857

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.