Evidence map›Paper›PMID 31664757›Full record

ReviewStem cells (Dayton, Ohio)2020

Inherited cardiac diseases, pluripotent stem cells, and genome editing combined-the past, present, and future.

Lettine van den Brink, Catarina Grandela, Christine L Mummery, Richard P Davis

Open access · bronzeAbstract readReview
In one paragraph

Review in Stem cells (Dayton, Ohio), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

21 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Article
  3. Multiplexed Functional Assessments ofCirculation. Genomic and precision medicine · 2024
    Article
  4. Review
  5. Article
  6. Article
  7. Genome Editing and Myocardial Development.Advances in experimental medicine and biology · 2023
    Review
  8. Article
  9. Review
  10. Article
  11. How Functional Genomics Can Keep Pace With VUS Identification.Frontiers in cardiovascular medicine · 2022
    Review
  12. Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. 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

4 authors at 1 institution in 1 country.

Lettine van den BrinkDepartment of Anatomy and Embryology, Leiden University Medical Center, RC Leiden, The Netherlands.
Catarina GrandelaDepartment of Anatomy and Embryology, Leiden University Medical Center, RC Leiden, The Netherlands.
Christine L MummeryDepartment of Anatomy and Embryology, Leiden University Medical Center, RC Leiden, The Netherlands.
Richard P DavisDepartment of Anatomy and Embryology, Leiden University Medical Center, RC Leiden, The Netherlands.ORCID 0000-0002-7917-9423
Leiden University Medical Center · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Research on mechanisms underlying monogenic cardiac diseases such as primary arrhythmias and cardiomyopathies has until recently been hampered by inherent limitations of heterologous cell systems, where mutant genes are expressed in noncardiac cells, and physiological differences between humans and experimental animals. Human-induced pluripotent stem cells (hiPSCs) have proven to be a game changer by providing new opportunities for studying the disease in the specific cell type affected, namely the cardiomyocyte. hiPSCs are particularly valuable because not only can they be differentiated into unlimited numbers of these cells, but they also genetically match the individual from whom they were derived. The decade following their discovery showed the potential of hiPSCs for advancing our understanding of cardiovascular diseases, with key pathophysiological features of the patient being reflected in their corresponding hiPSC-derived cardiomyocytes (the past). Now, recent advances in genome editing for repairing or introducing genetic mutations efficiently have enabled the disease etiology and pathogenesis of a particular genotype to be investigated (the present). Finally, we are beginning to witness the promise of hiPSC in personalized therapies for individual patients, as well as their application in identifying genetic variants responsible for or modifying the disease phenotype (the future). In this review, we discuss how hiPSCs could contribute to improving the diagnosis, prognosis, and treatment of an individual with a suspected genetic cardiac disease, thereby developing better risk stratification and clinical management strategies for these potentially lethal but treatable disorders.

Indexed as

Cell DifferentiationGene EditingHeart DiseasesHumansPluripotent Stem CellscardiacCRISPRdifferentiationexperimental modelsgene targetingpluripotent stem cells

Identifiers

PMID31664757
PMCPMC7027796
OpenAlexW2982341188

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.