Evidence map›Paper›PMID 27074686›Full record

ArticleBiophysical journal2016

Emergent Global Contractile Force in Cardiac Tissues.

Meghan B Knight, Nancy K Drew, Linda A McCarthy, Anna Grosberg

Abstract read
In one paragraph

Article in Biophysical journal, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed.

  1. Article
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  4. Article
  5. Review
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  9. Article
  10. Engineering cardiac microphysiological systems to model pathological extracellular matrix remodeling.American journal of physiology. Heart and circulatory physiology · 2018
    Review
  11. Article
  12. Article
  13. Article
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  16. 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

4 authors.

Meghan B KnightDepartment of Biomedical Engineering, University of California-Irvine, Irvine, California; Center for Complex Biological Systems, University of California-Irvine, Irvine, California.
Nancy K DrewDepartment of Biomedical Engineering, University of California-Irvine, Irvine, California; Center for Complex Biological Systems, University of California-Irvine, Irvine, California; The Edwards Lifesciences Center for Advanced Cardiovascular Technology, University of California-Irvine, Irvine, California.
Linda A McCarthyDepartment of Biomedical Engineering, University of California-Irvine, Irvine, California; Center for Complex Biological Systems, University of California-Irvine, Irvine, California.
Anna GrosbergDepartment of Biomedical Engineering, University of California-Irvine, Irvine, California; Department of Chemical and Biochemical Engineering and Materials Science, University of California-Irvine, Irvine, California; Center for Complex Biological Systems, University of California-Irvine, Irvine, California; The Edwards Lifesciences Center for Advanced Cardiovascular Technology, University of California-Irvine, Irvine, California. Electronic address: grosberg@uci.edu.

Funding

Mathematical, Computational and Systems BiologyT32EB009418 · NIBIB · UNIVERSITY OF CALIFORNIA-IRVINE · PI LANDER, ARTHUR D, NIE, QING · 2009 to 2019
$2.4M
NIBIB NIH HHS T32 EB009418
6 · The paper itself

Abstract

The heart is a complex organ whose structure and function are intricately linked at multiple length scales. Although several advancements have been achieved in the field of cardiac tissue engineering, current in vitro cardiac tissues do not fully replicate the structure or function necessary for effective cardiac therapy and cardiotoxicity studies. This is partially due to a deficiency in current understandings of cardiac tissue organization's potential downstream effects, such as changes in gene expression levels. We developed a novel (to our knowledge) in vitro tool that can be used to decouple and quantify the contribution of organization and associated downstream effects to tissue function. To do so, cardiac tissue monolayers were designed into a parquet pattern to be organized anisotropically on a local scale, within a parquet tile, and with any desired organization on a global scale. We hypothesized that if the downstream effects were muted, the relationship between developed force and tissue organization could be modeled as a sum of force vectors. With the in vitro experimental platforms of parquet tissues and heart-on-a-chip devices, we were able to prove this hypothesis for both systolic and diastolic stresses. Thus, insight was gained into the relationship between the generated stress and global myofibril organization. Furthermore, it was demonstrated that the developed quantitative tool could be used to estimate the changes in stress production due to downstream effects decoupled from tissue architecture. This has the potential to elucidate properties coupled to tissue architecture, which change force production and pumping function in the diseased heart or stem cell-derived tissues.

Indexed as

Mechanical PhenomenaMyocardial ContractionAnimalsBiomechanical PhenomenaMyocardiumRats

Identifiers

PMID27074686
PMCPMC4833833

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.