Evidence map›Paper›PMID 23716679›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2013

Recapitulating maladaptive, multiscale remodeling of failing myocardium on a chip.

Megan L McCain, Sean P Sheehy, Anna Grosberg, Josue A Goss, Kevin Kit Parker

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed
16.0field-weighted citation impact, top 1% 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

84 citing papers in PubMed, 157 citations in OpenAlex.

  1. Review
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  6. Stimuli-responsive hybrid materials for 4DMaterials today. Bio · 2025
    Review
  7. Organs on chips: fundamentals, bioengineering and applications.Journal of artificial organs : the official journal of the Japanese Society for Artificial Organs · 2025
    Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. Review
  13. The Utilisation of Hydrogels for iPSC-Cardiomyocyte Research.International journal of molecular sciences · 2023
    Review
  14. Organ Chips and Visualization of Biological Systems.Advances in experimental medicine and biology · 2023
    Article
  15. Cardiac Disease Modeling with Engineered Heart Tissue.Handbook of experimental pharmacology · 2023
    Review
  16. Article
  17. Article
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  19. Article
  20. Review

24 more citing papers are in PubMed but not listed here.

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

5 authors at 1 institution in 1 country.

Megan L McCainDisease Biophysics Group, Wyss Institute for Biologically Inspired Engineering, School of Engineering and Applied Sciences, Harvard University, Cambridge, MA 02138, USA.
Sean P Sheehy
Anna Grosberg
Josue A Goss
Kevin Kit Parker
Harvard University · US

Funding

Human Cardio-Pulmonary System on a ChipUH3TR000522 · NCATS · HARVARD MEDICAL SCHOOL · PI PARKER, KEVIN KIT · 2014 to 2016
$3.6M
Human Cardio-Pulmonary System on a ChipUH2TR000522 · NCATS · HARVARD MEDICAL SCHOOL · PI PARKER, KEVIN KIT · 2012 to 2013
$2.4M
Myocyte Shape in Myofibril Patterning and ContractionR01HL079126 · NHLBI · HARVARD UNIVERSITY · PI PARKER, KEVIN KIT · 2007 to 2010
$1.4M
NCATS NIH HHS 1 UH2 TR000522-01NCATS NIH HHS UH2 TR000522NCATS NIH HHS UH3 TR000522NHLBI NIH HHS 1 R01HL079126NHLBI NIH HHS R01 HL079126
6 · The paper itself

Abstract

The lack of a robust pipeline of medical therapeutic agents for the treatment of heart disease may be partially attributed to the lack of in vitro models that recapitulate the essential structure-function relationships of healthy and diseased myocardium. We designed and built a system to mimic mechanical overload in vitro by applying cyclic stretch to engineered laminar ventricular tissue on a stretchable chip. To test our model, we quantified changes in gene expression, myocyte architecture, calcium handling, and contractile function and compared our results vs. several decades of animal studies and clinical observations. Cyclic stretch activated gene expression profiles characteristic of pathological remodeling, including decreased α- to β-myosin heavy chain ratios, and induced maladaptive changes to myocyte shape and sarcomere alignment. In stretched tissues, calcium transients resembled those reported in failing myocytes and peak systolic stress was significantly reduced. Our results suggest that failing myocardium, as defined genetically, structurally, and functionally, can be replicated in an in vitro microsystem by faithfully recapitulating the structural and mechanical microenvironment of the diseased heart.

Indexed as

AnimalsAnimals, NewbornCalciumCells, CulturedGene Expression ProfilingHeart FailureHumansModels, CardiovascularMyocardial ContractionMyocardiumMyocytes, CardiacMyosin Heavy ChainsOligonucleotide Array Sequence AnalysisRats, Sprague-DawleySarcomeresSystoleCalciumMyosin Heavy ChainsVentricular Myosinscontractionmechanotransductionmicroarraymuscular thin filmsorgans on chips

Identifiers

PMID23716679
PMCPMC3683774
OpenAlexW2079176005

What OpenQuestion holds

Textmetadata
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.