Evidence map›Paper›PMID 25618410›Full record

ReviewCardiovascular research2015

Modelling sarcomeric cardiomyopathies in the dish: from human heart samples to iPSC cardiomyocytes.

Thomas Eschenhagen, Christine Mummery, Bjorn C Knollmann

Open access · hybridAbstract readReview
In one paragraph

Review in Cardiovascular research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 1 pooled it
7.9field-weighted citation impact, top 2% 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

52 citing papers in PubMed, 1 synthesis or guideline pooled it, 94 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Cardiac troponin T N-domain variant destabilizes the actin interface resulting in disturbed myofilament function.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  13. Transcriptome studies of inherited dilated cardiomyopathies.Mammalian genome : official journal of the International Mammalian Genome Society · 2023
    Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Application of hiPSC as a Drug TesterFrontiers in genetics · 2022
    Review
  19. Article
  20. Alpha and beta myosin isoforms and human atrial and ventricular contraction.Cellular and molecular life sciences : CMLS · 2021
    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 3 institutions in 3 countries.

Thomas EschenhagenDepartment of Experimental Pharmacology and Toxicology, University Medical Center Hamburg Eppendorf, Martinistr. 52, 20246 Hamburg, Germany DZHK (German Centre for Cardiovascular Research), Partner Site Hamburg/Kiel/Lübeck t.eschenhagen@uke.de bjorn.knollmann@vanderbilt.edu.
Christine MummeryDepartment of Anatomy and Embryology, Leiden University Medical Centre, Einthovenweg 20, 2333ZC Leiden, The Netherlands.
Bjorn C KnollmannDivision of Clinical Pharmacology, Department of Medicine, Vanderbilt University School of Medicine, 2215 Garland Ave, Nashville, TN 37232, USA t.eschenhagen@uke.de bjorn.knollmann@vanderbilt.edu.
German Centre for Cardiovascular Research · DELeiden University · NLVanderbilt University · US

Funding

Troponin T mutations and Sudden Cardiac DeathR01HL071670 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI KNOLLMANN, BJORN C · 2003 to 2017
$4.5M
Calsequestrin in Ventricular Arrhythmia and Sudden DeathR01HL088635 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI KNOLLMANN, BJORN C · 2007 to 2015
$3.2M
NHLBI NIH HHS HL71670NHLBI NIH HHS R01 HL071670NHLBI NIH HHS R01 HL88635
6 · The paper itself

Abstract

One of the obstacles to a better understanding of the pathogenesis of human cardiomyopathies has been poor availability of heart-tissue samples at early stages of disease development. This has possibly changed by the advent of patient-derived induced pluripotent stem cell (hiPSC) from which cardiomyocytes can be derived in vitro. The main promise of hiPSC technology is that by capturing the effects of thousands of individual gene variants, the phenotype of differentiated derivatives of these cells will provide more information on a particular disease than simple genotyping. This article summarizes what is known about the 'human cardiomyopathy or heart failure phenotype in vitro', which constitutes the reference for modelling sarcomeric cardiomyopathies in hiPSC-derived cardiomyocytes. The current techniques for hiPSC generation and cardiac myocyte differentiation are briefly reviewed and the few published reports of hiPSC models of sarcomeric cardiomyopathies described. A discussion of promises and challenges of hiPSC-modelling of sarcomeric cardiomyopathies and individualized approaches is followed by a number of questions that, in the view of the authors, need to be answered before the true potential of this technology can be evaluated.

Indexed as

Cell DifferentiationModels, CardiovascularAnimalsCardiomyopathiesCells, CulturedGenetic MarkersGenetic Predisposition to DiseaseHumansInduced Pluripotent Stem CellsMutationMyocytes, CardiacPhenotypeSarcomeresTranslational Research, BiomedicalGenetic MarkersDisease modelingDisease phenotypeHeart FailureInduced pluripotent stem cellsSarcomeric cardiomyopathy

Identifiers

PMID25618410
PMCPMC4349163
OpenAlexW2115177875

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.