Evidence map›Paper›PMID 24054750›Full record

ReviewTrends in cardiovascular medicine2014

Modeling heart disease in a dish: from somatic cells to disease-relevant cardiomyocytes.

Fabian Zanella, Robert C Lyon, Farah Sheikh

Open access · greenAbstract readReview
In one paragraph

Review in Trends in cardiovascular medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

12 citing papers in PubMed, 23 citations in OpenAlex.

  1. Towards Improved HumanBiomedicines · 2023
    Review
  2. Review
  3. Article
  4. Article
  5. Biology of the cardiac myocyte in heart disease.Molecular biology of the cell · 2016
    Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Organ-on-a-chip platforms for studying drug delivery systems.Journal of controlled release : official journal of the Controlled Release Society · 2014
    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.

Fabian ZanellaDepartment of Medicine (Cardiology Division), University of California-San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA.
Robert C LyonDepartment of Medicine (Cardiology Division), University of California-San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA.
Farah SheikhDepartment of Medicine (Cardiology Division), University of California-San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA. Electronic address: fasheikh@ucsd.edu.
University of California, San Diego · US

Funding

Training In Cardiovascular Physiology & PharmacologyT32HL007444 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Ju Chen, Robert Scott Ross · 1985 to 2026
$11.1M
The molecular mechanisms underlying arrhythmogenic right ventricular dysplasia/cardiomyopathyR01HL095780 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI SHEIKH, FARAH · 2009 to 2018
$3.9M
NHLBI NIH HHS R01 HL095780NHLBI NIH HHS T32 HL007444
6 · The paper itself

Abstract

A scientific milestone that has tremendously impacted the cardiac research field has been the discovery and establishment of human-induced pluripotent stem cells (hiPSC). Key to this discovery has been uncovering a viable path in generating human patient and disease-specific cardiac cells to dynamically model and study human cardiac diseases in an in vitro setting. Recent studies have demonstrated that hiPSC-derived cardiomyocytes can be used to model and recapitulate various known disease features in hearts of patient donors harboring genetic-based cardiac diseases. Experimental drugs have also been tested in this setting and shown to alleviate disease phenotypes in hiPSC-derived cardiomyocytes, further paving the way for therapeutic interventions for cardiac disease. Here, we review state-of-the-art methods to generate high-quality hiPSC and differentiate them towards cardiomyocytes as well as the full range of genetic-based cardiac diseases, which have been modeled using hiPSC. We also provide future perspectives on exploiting the potential of hiPSC to compliment existing studies and gain new insights into the mechanisms underlying cardiac disease.

Indexed as

Cell DifferentiationCell LineageAnimalsCells, CulturedGene Expression Regulation, DevelopmentalHeart DiseasesHumansInduced Pluripotent Stem CellsMyocytes, CardiacPhenotypeSignal Transduction

Identifiers

PMID24054750
PMCPMC4969049
OpenAlexW2025187846

What OpenQuestion holds

Textmetadata
LicenceTDM
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.