Evidence map›Paper›PMID 31754410›Full record

ReviewWorld journal of cardiology2019

Cellular models for human cardiomyopathy: What is the best option?

Nerea Jimenez-Tellez, Steven C Greenway

Abstract readReview
In one paragraph

Review in World journal of cardiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
–field-weighted citation impact
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

18 citing papers in PubMed.

  1. A Novel Pak1 Activator Ameliorates ER Stress for HFpEF Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
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  5. Article
  6. Review
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  11. Cardiac tissue engineering: Multiple approaches and potential applications.Frontiers in bioengineering and biotechnology · 2022
    Review
  12. Review
  13. Review
  14. Article
  15. Frontiers in physiology · 2021
    Review
  16. Human Cell Modeling for Cardiovascular Diseases.International journal of molecular sciences · 2020
    Review
  17. Article
  18. 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

2 authors.

Nerea Jimenez-TellezDepartment of Biochemistry & Molecular Biology, Cumming School of Medicine, University of Calgary, Calgary, AB T2N 4N1, Canada.
Steven C GreenwayDepartments of Pediatrics, Cardiac Sciences, Biochemistry & Molecular Biology, Cumming School of Medicine, Libin Cardiovascular Institute of Alberta, Alberta Children's Hospital Research Institute, University of Calgary, Calgary, AB T2N 4N1, Canada. scgreenw@ucalgary.ca.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The genetic cardiomyopathies are a group of disorders related by abnormal myocardial structure and function. Although individually rare, these diseases collectively represent a significant health burden since they usually develop early in life and are a major cause of morbidity and mortality amongst affected children. The heterogeneity and rarity of these disorders requires the use of an appropriate model system in order to characterize the mechanism of disease and develop useful therapeutics since standard drug trials are infeasible. A common approach to study human disease involves the use of animal models, especially rodents, but due to important biological and physiological differences, this model system may not recapitulate human disease. An alternative approach for studying the metabolic cardiomyopathies relies on the use of cellular models which have most frequently been immortalized cell lines or patient-derived fibroblasts. However, the recent introduction of induced pluripotent stem cells (iPSCs), which have the ability to differentiate into any cell type in the body, is of great interest and has the potential to revolutionize the study of rare diseases. In this paper we review the advantages and disadvantages of each model system by comparing their utility for the study of mitochondrial cardiomyopathy with a particular focus on the use of iPSCs in cardiovascular biology for the modeling of rare genetic or metabolic diseases.

Indexed as

CardiomyopathyCellular modelsFibroblastsInduced pluripotent stem cellsMitochondria

Identifiers

PMID31754410
PMCPMC6859298

What OpenQuestion holds

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Registered trials

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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.