Evidence map›Paper›PMID 28823079›Full record

ArticleBiomechanics and modeling in mechanobiology2018

Mechanobiological model of arterial growth and remodeling.

Maziyar Keshavarzian, Clark A Meyer, Heather N Hayenga

Abstract read
In one paragraph

Article in Biomechanics and modeling in mechanobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing 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

19 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Guidelines for mechanistic modeling and analysis in cardiovascular research.American journal of physiology. Heart and circulatory physiology · 2024
    Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. [Review of studies on the biomechanical modelling of the coupling effect between stent degradation and blood vessel remodeling].Sheng wu yi xue gong cheng xue za zhi = Journal of biomedical engineering = Shengwu yixue gongchengxue zazhi · 2020
    Article
  12. Article
  13. Review
  14. A computational bio-chemo-mechanical model of in vivo tissue-engineered vascular graft development.Integrative biology : quantitative biosciences from nano to macro · 2020
    Article
  15. Article
  16. Tissue engineering. Part C, Methods · 2019
    Article
  17. Article
  18. Uncertainty Quantification of a Multiscale Model for In-Stent Restenosis.Cardiovascular engineering and technology · 2018
    Article
  19. Bio-chemo-mechanics of thoracic aortic aneurysms.Current opinion in biomedical engineering · 2018
    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

3 authors.

Maziyar KeshavarzianDepartment of Biomedical Engineering, The University of Texas at Dallas, 800 W. Campbell Road, Richardson, TX, 75080, USA.ORCID 0000-0001-5923-8425
Clark A MeyerDepartment of Biomedical Engineering, The University of Texas at Dallas, 800 W. Campbell Road, Richardson, TX, 75080, USA.
Heather N HayengaDepartment of Biomedical Engineering, The University of Texas at Dallas, 800 W. Campbell Road, Richardson, TX, 75080, USA. heather.hayenga@utdallas.edu.ORCID 0000-0001-7581-8294

Funding

A computational model of the G&R during atherosclerosis: Integrating mechanics and biologyR01HL136776 · NHLBI · UNIVERSITY OF TEXAS DALLAS · PI HAYENGA, HEATHER NAOMI · 2018 to 2022
$1.9M
American Heart Association 17SDG33400239NHLBI NIH HHS R01 HL136776
6 · The paper itself

Abstract

A coupled agent-based model (ABM) and finite element analysis (FEA) computational framework is developed to study the interplay of bio-chemo-mechanical factors in blood vessels and their role in maintaining homeostasis. The agent-based model implements the power of REPAST Simphony libraries and adapts its environment for biological simulations. Coupling a continuum-level model (FEA) to a cellular-level model (ABM) has enabled this computational framework to capture the response of blood vessels to increased or decreased levels of growth factors, proteases and other signaling molecules (on the micro scale) as well as altered blood pressure. Performance of the model is assessed by simulating porcine left anterior descending artery under normotensive conditions and transient increases in blood pressure and by analyzing sensitivity of the model to variations in the rule parameters of the ABM. These simulations proved that the model is stable under normotensive conditions and can recover from transient increases in blood pressure. Sensitivity studies revealed that the model is most sensitive to variations in the concentration of growth factors that affect cellular proliferation and regulate extracellular matrix composition (mainly collagen).

Indexed as

Models, CardiovascularVascular RemodelingAdventitiaAnimalsArteriesBiomechanical PhenomenaBlood PressureExtracellular MatrixFinite Element AnalysisMiceStress, MechanicalSus scrofaSystems AnalysisUser-Computer InterfaceAgent-based modelingCoronary arteryFinite element analysisMultiscale modeling

Identifiers

PMID28823079
PMCPMC6292683

What OpenQuestion holds

Textmetadata
LicenceTDM
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.