Evidence map›Paper›PMID 19132116›Full record

ReviewDisease models & mechanisms

Fishing for the genetic basis of cardiovascular disease.

Tillman Dahme, Hugo A Katus, Wolfgang Rottbauer

Open access · bronzeAbstract readReview
In one paragraph

Review in Disease models & mechanisms. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

35 citing papers in PubMed, 75 citations in OpenAlex.

  1. Article
  2. An inherited life-threatening arrhythmia model established by screening randomly mutagenized mice.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  3. Article
  4. Review
  5. Zebrafish Heart Failure Models.Frontiers in cell and developmental biology · 2021
    Review
  6. Article
  7. Article
  8. Article
  9. Genetics of Cardiovascular Disease: Fishing for Causality.Frontiers in cardiovascular medicine · 2018
    Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Fish is Fish: the use of experimental model species to reveal causes of skeletal diversity in evolution and disease.Zeitschrift fur angewandte Ichthyologie = Journal of applied ichthyology · 2014
    Article
  18. Genetics and disease of ventricular muscle.Cold Spring Harbor perspectives in medicine · 2014
    Review
  19. Article
  20. 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 at 1 institution in 1 country.

Tillman DahmeDepartment of Medicine III, University of Heidelberg, Heidelberg, Germany.
Hugo A Katus
Wolfgang Rottbauer
Heidelberg University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiovascular disease (CVD) has recently overtaken infectious disease to become the biggest global killer. Genetic factors have emerged as being of major importance in the pathogenesis of CVD. Owing to disease heterogeneity, variable penetrance and high mortality, human genetic studies alone are not sufficient to elucidate the genetic basis of CVD. Animal models are needed to identify novel genes that are involved in cardiovascular pathology and to verify the effect of suspected disease genes on cardiovascular function. An intriguing model organism is the zebrafish danio rerio. Several features of the zebrafish, such as a closed cardiovascular system, transparency at embryonal stages, rapid and external development, and easily tractable genetics make it ideal for cardiovascular research. Moreover, zebrafish are suitable for forward genetics approaches, which allow the unbiased identification of novel and unanticipated cardiovascular genes. Zebrafish mutants with various cardiovascular phenotypes that closely correlate with human disease, such as congenital heart disease, cardiomyopathies and arrhythmias, have been isolated. The pool of zebrafish mutants, for which the causal gene mutation has been identified, is constantly growing. The human orthologues of several of these zebrafish genes have been shown to be involved in the pathogenesis of human CVD. Cardiovascular zebrafish models also provide the opportunity to develop and test novel therapeutic strategies, using innovative technologies such as high throughput in vivo small molecule screens.

Indexed as

Disease Models, AnimalAnimalsAnimals, Genetically ModifiedArrhythmias, CardiacCardiomyopathiesCardiovascular DiseasesGene Expression RegulationHeartHumansMutagenesisMutationPhenotypeZebrafishZebrafish ProteinsZebrafish Proteins

Identifiers

PMID19132116
PMCPMC2615162
OpenAlexW2011498457

What OpenQuestion holds

Textmetadata
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.