Evidence map›Paper›PMID 30624779›Full record

ReviewThe Journal of physiology2020

Modelling sarcomeric cardiomyopathies with human cardiomyocytes derived from induced pluripotent stem cells.

Lorenzo R Sewanan, Stuart G Campbell

Abstract readReview
In one paragraph

Review in The Journal of physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing 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

24 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. A transcriptional enhancer regulates cardiac maturation.Nature cardiovascular research · 2024
    Article
  5. Article
  6. Article
  7. Transcriptome studies of inherited dilated cardiomyopathies.Mammalian genome : official journal of the International Mammalian Genome Society · 2023
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Maturing heart muscle cells: Mechanisms and transcriptomic insights.Seminars in cell & developmental biology · 2021
    Review
  16. Article
  17. Review
  18. Article
  19. Silencing ofPhysiological genomics · 2020
    Article
  20. Contractile work directly modulates mitochondrial protein levels in human engineered heart tissues.American journal of physiology. Heart and circulatory physiology · 2020
    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.

Lorenzo R SewananDepartment of Biomedical Engineering, Yale University, New Haven, CT, USA.ORCID 0000-0003-2629-1865
Stuart G CampbellDepartment of Biomedical Engineering, Yale University, New Haven, CT, USA.ORCID 0000-0002-1527-0770

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM007205 · NIGMS · YALE UNIVERSITY · PI KAZMIERCZAK, BARBARA I · 1985 to 2019
$42.9M
Revealing Pathomechanisms of Mutant TPM1 Through a Hybrid Computational-Experimental ApproachR01HL136590 · NHLBI · YALE UNIVERSITY · PI STUART G CAMPBELL, William J Lehman · 2017 to 2026
$5.6M
HHS | National Institutes of Health (NIH) HL136590HHS | National Institutes of Health (NIH) T32GM007205NHLBI NIH HHS R01 HL136590NIGMS NIH HHS T32 GM007205NIH HHS HL136590NIH HHS T32GM007205Paul and Daisy Soros Fellowship for New Americans
6 · The paper itself

Abstract

Cardiomyocytes derived from human induced pluripotent stem cells (iPSCs) provide a unique opportunity to understand the pathophysiological effects of genetic cardiomyopathy mutations. In particular, these cells hold the potential to unmask the effects of mutations on contractile behaviour in vitro, providing new insights into genotype-phenotype relationships. With this goal in mind, several groups have established iPSC lines that contain sarcomeric gene mutations linked to cardiomyopathy in patient populations. Their studies have employed diverse systems and methods for performing mechanical measurements of contractility, ranging from single cell techniques to multicellular tissue-like constructs. Here, we review published results to date within the growing field of iPSC-based sarcomeric cardiomyopathy disease models. We devote special attention to the methods of mechanical characterization selected in each case, and how these relate to the paradigms of classical muscle mechanics. An appreciation of these somewhat subtle paradigms can inform efforts to compare the results of different studies and possibly reconcile discrepancies. Although more work remains to be done to improve and possibly standardize methods for producing, maturing, and mechanically interrogating iPSC-derived cardiomyocytes, the initial results indicate that this approach to modelling cardiomyopathies will continue to provide critical insights into these devastating diseases.

Indexed as

CardiomyopathiesInduced Pluripotent Stem CellsCell DifferentiationHumansMutationMyocytes, CardiacSarcomerescardiac mechanicsengineered heart tissueHypertrophic cardiomyopathyiPSC-derived Cardiomyocytesarcomeric mutations

Identifiers

PMID30624779
PMCPMC8208589

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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.