Evidence map›Paper›PMID 18343897›Full record

ArticleCardiovascular research2008

Depletion of zebrafish essential and regulatory myosin light chains reduces cardiac function through distinct mechanisms.

Zhenyue Chen, Wei Huang, Tillman Dahme, Wolfgang Rottbauer, Michael J Ackerman, Xiaolei Xu

Open access · bronzeAbstract read
In one paragraph

Article in Cardiovascular research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

51 citing papers in PubMed, 122 citations in OpenAlex.

  1. Versatile CRISPR-Cas Tools for Gene Regulation in Zebrafish via an Enhanced Q Binary System.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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  14. Regulatory Light Chains in Cardiac Development and Disease.International journal of molecular sciences · 2021
    Review
  15. Mechanisms ofJournal of cardiovascular development and disease · 2021
    Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. The Genetic Puzzle of Familial Atrial Fibrillation.Frontiers in cardiovascular medicine · 2020
    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

6 authors at 2 institutions in 3 countries.

Zhenyue ChenDepartment of Cardiology, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Wei Huang
Tillman Dahme
Wolfgang Rottbauer
Michael J Ackerman
Xiaolei Xu
Mayo Clinic · USHeidelberg University · DE

Funding

Genetic Studies of Sarcomere-based Cardiac Diseases (Diversity Supplement)R01HL081753 · NHLBI · MAYO CLINIC ROCHESTER · PI XU, XIAOLEI · 2005 to 2025
$7.8M
NHLBI NIH HHS HL81753NHLBI NIH HHS R01 HL081753
6 · The paper itself

Abstract

aimsMutations in the essential myosin light chain (ELC) and regulatory myosin light chain (RLC) genes have been linked to sarcomeric hypertrophic cardiomyopathies in humans; however, the specific functions of the different myosin light chains during cardiogenesis in a vertebrate animal are not well understood. METHODS AND

resultsUsing zebrafish (Danio rerio) as a model organism, we have identified cmlc1 and cmlc2 as the main ELC and RLC orthologues, respectively, and have furthermore characterized their functions during cardiogenesis by morpholino technology. Depletion of either cmlc1 or cmlc2 using morpholino-modified antisense oligonucleotides leads to a disruption in sarcomere structure and compromises cardiac function as well, although through seemingly distinct mechanisms. While myosin still assembles into a novel rod-like structure in both morphants, the sarcomere length is longer in cmlc1 morphants than that in wild-type embryos, whereas it is shorter in cmlc2 morphants. In addition, cardiomyocyte size and number are increased upon depletion of cmlc1, resulting in a larger ventricular chamber volume; in contrast, depletion of cmlc2 leads to a reduction in cardiomyocyte size and number.

conclusionOur data have elucidated distinct roles for cmlc1 and cmlc2 during zebrafish cardiogenesis, suggesting that cardiomyopathies resulting from human mutations in ELCs vs. RLCs may have distinct pathological characteristics during disease progression.

Indexed as

AnimalsCardiac MyosinsCardiomyopathiesCell CountCell SizeDisease Models, AnimalHeartMutationMyocardiumMyocytes, CardiacMyosin Light ChainsOligoribonucleotides, AntisenseSarcomeresZebrafishZebrafish ProteinsCardiac MyosinsCmlc1 protein, zebrafishmyl7 protein, zebrafishMyosin Light ChainsOligoribonucleotides, AntisenseZebrafish Proteins

Identifiers

PMID18343897
PMCPMC2724891
OpenAlexW2150379181

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.