Evidence map›Paper›PMID 26808388›Full record

ArticlePloS one2016

Angiotensin II Induced Cardiac Dysfunction on a Chip.

Renita E Horton, Moran Yadid, Megan L McCain, Sean P Sheehy, Francesco S Pasqualini, Sung-Jin Park, Alexander Cho, Patrick Campbell, Kevin Kit Parker

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

18 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Intersection of stem cell biology and engineering towards next generationFrontiers in bioengineering and biotechnology · 2022
    Review
  9. Review
  10. Article
  11. The Right Ventricle in COVID-19.Journal of clinical medicine · 2021
    Review
  12. Organs-on-chips: into the next decade.Nature reviews. Drug discovery · 2021
    Review
  13. Review
  14. Considerations for anFrontiers in pharmacology · 2019
    Review
  15. Review
  16. Review
  17. Chymase-dependent production of angiotensin II: an old enzyme in old hearts.American journal of physiology. Heart and circulatory physiology · 2017
    Article
  18. 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

9 authors at 1 institution in 1 country.

Renita E HortonDisease Biophysics Group, Wyss Institute for Biologically Inspired Engineering, John A. Paulson School of Engineering and Applied Sciences, Harvard University, Cambridge, Massachusetts, United States of America.
Moran YadidDisease Biophysics Group, Wyss Institute for Biologically Inspired Engineering, John A. Paulson School of Engineering and Applied Sciences, Harvard University, Cambridge, Massachusetts, United States of America.
Megan L McCainDisease Biophysics Group, Wyss Institute for Biologically Inspired Engineering, John A. Paulson School of Engineering and Applied Sciences, Harvard University, Cambridge, Massachusetts, United States of America.
Sean P SheehyDisease Biophysics Group, Wyss Institute for Biologically Inspired Engineering, John A. Paulson School of Engineering and Applied Sciences, Harvard University, Cambridge, Massachusetts, United States of America.
Francesco S PasqualiniDisease Biophysics Group, Wyss Institute for Biologically Inspired Engineering, John A. Paulson School of Engineering and Applied Sciences, Harvard University, Cambridge, Massachusetts, United States of America.
Sung-Jin ParkDisease Biophysics Group, Wyss Institute for Biologically Inspired Engineering, John A. Paulson School of Engineering and Applied Sciences, Harvard University, Cambridge, Massachusetts, United States of America.
Alexander ChoDisease Biophysics Group, Wyss Institute for Biologically Inspired Engineering, John A. Paulson School of Engineering and Applied Sciences, Harvard University, Cambridge, Massachusetts, United States of America.
Patrick CampbellDisease Biophysics Group, Wyss Institute for Biologically Inspired Engineering, John A. Paulson School of Engineering and Applied Sciences, Harvard University, Cambridge, Massachusetts, United States of America.
Kevin Kit ParkerDisease Biophysics Group, Wyss Institute for Biologically Inspired Engineering, John A. Paulson School of Engineering and Applied Sciences, Harvard University, Cambridge, Massachusetts, United States of America.
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
NCATS NIH HHS 1 UH2 TR000522-01NCATS NIH HHS 4 UH3TR000522-03NCATS NIH HHS UH2 TR000522NCATS NIH HHS UH3 TR000522
6 · The paper itself

Abstract

In vitro disease models offer the ability to study specific systemic features in isolation to better understand underlying mechanisms that lead to dysfunction. Here, we present a cardiac dysfunction model using angiotensin II (ANG II) to elicit pathological responses in a heart-on-a-chip platform that recapitulates native laminar cardiac tissue structure. Our platform, composed of arrays of muscular thin films (MTF), allows for functional comparisons of healthy and diseased tissues by tracking film deflections resulting from contracting tissues. To test our model, we measured gene expression profiles, morphological remodeling, calcium transients, and contractile stress generation in response to ANG II exposure and compared against previous experimental and clinical results. We found that ANG II induced pathological gene expression profiles including over-expression of natriuretic peptide B, Rho GTPase 1, and T-type calcium channels. ANG II exposure also increased proarrhythmic early after depolarization events and significantly reduced peak systolic stresses. Although ANG II has been shown to induce structural remodeling, we control tissue architecture via microcontact printing, and show pathological genetic profiles and functional impairment precede significant morphological changes. We assert that our in vitro model is a useful tool for evaluating tissue health and can serve as a platform for studying disease mechanisms and identifying novel therapeutics.

Indexed as

Angiotensin IIAnimalsGene ExpressionGene Expression ProfilingModels, TheoreticalMyocardial ContractionMyocardiumMyocytes, CardiacRatsVentricular RemodelingAngiotensin II

Identifiers

PMID26808388
PMCPMC4725954
OpenAlexW2271737778

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.