Evidence map›Paper›PMID 22594976›Full record

ArticleBiomaterials2012

Controlling the contractile strength of engineered cardiac muscle by hierarchal tissue architecture.

Adam W Feinberg, Patrick W Alford, Hongwei Jin, Crystal M Ripplinger, Andreas A Werdich, Sean P Sheehy, Anna Grosberg, Kevin Kit Parker

Abstract read
In one paragraph

Article in Biomaterials, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 126 papers.

0numbers the graph read from it
0cells of the map it votes in
126citing 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

126 citing papers in PubMed.

  1. Article
  2. Review
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  4. Article
  5. Review
  6. Cardiac myofibril networks induce shear stress.NPJ systems biology and applications · 2026
    Article
  7. In vitro sex-specific function-structure relationship in neonatal rat cardiac monolayers.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

66 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

8 authors.

Adam W FeinbergDisease Biophysics Group, Harvard Stem Cell Institute, Wyss Institute of Biologically Inspired Engineering, School of Engineering and Applied Sciences, Harvard University, Cambridge, MA 02138, USA.
Patrick W Alford
Hongwei Jin
Crystal M Ripplinger
Andreas A Werdich
Sean P Sheehy
Anna Grosberg
Kevin Kit Parker

Funding

Human Pluripotent Stem Cell and Progenitor Models of Cardiac and Blood DiseasesU01HL100408 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI COWAN, CHAD ALBERT, MELTON, DOUGLAS A · 2009 to 2015
$8.9M
Myocyte Shape in Myofibril Patterning and ContractionR01HL079126 · NHLBI · HARVARD UNIVERSITY · PI PARKER, KEVIN KIT · 2007 to 2010
$1.4M
NHLBI NIH HHS R01 HL079126NHLBI NIH HHS U01 HL100408
6 · The paper itself

Abstract

The heart is a muscular organ with a wrapping, laminar structure embedded with neural and vascular networks, collagen fibrils, fibroblasts, and cardiac myocytes that facilitate contraction. We hypothesized that these non-muscle components may have functional benefit, serving as important structural alignment cues in inter- and intra-cellular organization of cardiac myocytes. Previous studies have demonstrated that alignment of engineered myocardium enhances calcium handling, but how this impacts actual force generation remains unclear. Quantitative assays are needed to determine the effect of alignment on contractile function and muscle physiology. To test this, micropatterned surfaces were used to build 2-dimensional myocardium from neonatal rat ventricular myocytes with distinct architectures: confluent isotropic (serving as the unaligned control), confluent anisotropic, and 20 μm spaced, parallel arrays of multicellular myocardial fibers. We combined image analysis of sarcomere orientation with muscular thin film contractile force assays in order to calculate the peak sarcomere-generated stress as a function of tissue architecture. Here we report that increasing peak systolic stress in engineered cardiac tissues corresponds with increasing sarcomere alignment. This change is larger than would be anticipated from enhanced calcium handling and increased uniaxial alignment alone. These results suggest that boundary conditions (heterogeneities) encoded in the extracellular space can regulate muscle tissue function, and that structural organization and cytoskeletal alignment are critically important for maximizing peak force generation.

Indexed as

Myocardial ContractionAnimalsCalciumCells, CulturedDimethylpolysiloxanesFibronectinsHeartMyocytes, CardiacRatsRats, Sprague-DawleySarcomeresTissue EngineeringTissue ScaffoldsbaysilonCalciumDimethylpolysiloxanesFibronectins

Identifiers

PMID22594976
PMCPMC4026933

What OpenQuestion holds

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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.