Evidence map›Paper›PMID 30030017›Full record

ArticleJournal of molecular and cellular cardiology2018

Network-based predictions of in vivo cardiac hypertrophy.

Deborah U Frank, Matthew D Sutcliffe, Jeffrey J Saucerman

Abstract read
In one paragraph

Article in Journal of molecular and cellular cardiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing 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

21 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Logic-based machine learning predicts how escitalopram attenuates cardiomyocyte hypertrophy.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  7. Global Sensitivity Analysis of a Novel Signaling Network for Heart Growth With Local IGF1 Production.International journal for numerical methods in biomedical engineering · 2025
    Article
  8. Article
  9. Article
  10. Computational model captures cardiac growth in hypertensive pregnancies and in the postpartum period.American journal of physiology. Heart and circulatory physiology · 2024
    Article
  11. Article
  12. Review
  13. Article
  14. Emerging therapeutic targets for cardiac hypertrophy.Expert opinion on therapeutic targets · 2022
    Review
  15. Review
  16. Article
  17. Article
  18. Computational models of cardiac hypertrophy.Progress in biophysics and molecular biology · 2021
    Review
  19. Article
  20. Computational model predicts paracrine and intracellular drivers of fibroblast phenotype after myocardial infarction.Matrix biology : journal of the International Society for Matrix Biology · 2020
    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.

Deborah U FrankDepartment of Biomedical Engineering, University of Virginia, Box 800759, Charlottesville 22908, VA, United States; Department of Pediatrics, University of Virginia, HSC Box 800386, Charlottesville 22908-0386, VA, United States. Electronic address: dcu2h@virginia.edu.
Matthew D SutcliffeDepartment of Biomedical Engineering, University of Virginia, Box 800759, Charlottesville 22908, VA, United States; Department of Pediatrics, University of Virginia, HSC Box 800386, Charlottesville 22908-0386, VA, United States. Electronic address: mds5cg@virginia.edu.
Jeffrey J SaucermanDepartment of Biomedical Engineering, University of Virginia, Box 800759, Charlottesville 22908, VA, United States. Electronic address: jjs3g@virginia.edu.

Funding

Multi-scale Systems Model of Murine Heart FailureR01HL105242 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BERS, DONALD M, MCCULLOCH, ANDREW D. · 2012 to 2016
$3.5M
Systems Biology of Hypertrophic Heart Disease from Molecular Pathways to Organ SystemR01HL137100 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI MCCULLOCH, ANDREW D. · 2017 to 2020
$2.0M
Systems Pharmacology Model for Spatial Control of Cardiac FibrosisR01HL137755 · NHLBI · UNIVERSITY OF VIRGINIA · PI HOLMES, JEFFREY W, SAUCERMAN, JEFFREY J. · 2017 to 2020
$1.9M
NHLBI NIH HHS R01 HL105242NHLBI NIH HHS R01 HL137100NHLBI NIH HHS R01 HL137755
6 · The paper itself

Abstract

Cardiac hypertrophy is a common response of cardiac myocytes to stress and a predictor of heart failure. While in vitro cell culture studies have identified numerous molecular mechanisms driving hypertrophy, it is unclear to what extent these mechanisms can be integrated into a consistent framework predictive of in vivo phenotypes. To address this question, we investigate the degree to which an in vitro-based, manually curated computational model of the hypertrophy signaling network is able to predict in vivo hypertrophy of 52 cardiac-specific transgenic mice. After minor revisions motivated by in vivo literature, the model concordantly predicts the qualitative responses of 78% of output species and 69% of signaling intermediates within the network model. Analysis of four double-transgenic mouse models reveals that the computational model robustly predicts hypertrophic responses in mice subjected to multiple, simultaneous perturbations. Thus the model provides a framework with which to mechanistically integrate data from multiple laboratories and experimental systems to predict molecular regulation of cardiac hypertrophy.

Indexed as

Angiotensin IIAnimalsCardiomegalyComputational BiologyDisease Models, AnimalHeart FailureHumansMiceMice, TransgenicMyocardiumMyocytes, CardiacSignal TransductionAngiotensin IICardiac hypertrophyComputational modelingHeart failureSystems biologyTransgenic mice

Identifiers

PMID30030017
PMCPMC6175293

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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.