Evidence map›Paper›PMID 23785479›Full record

ArticlePloS one2013

Modelling the effect of a functional endothelium on the development of in-stent restenosis.

Hannan Tahir, Carles Bona-Casas, Alfons G Hoekstra

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
5.5field-weighted citation impact, top 4% 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

28 citing papers in PubMed, 63 citations in OpenAlex.

  1. Article
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  7. Review
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  11. Semi-intrusive multiscale metamodelling uncertainty quantification with application to a model of in-stent restenosis.Philosophical transactions. Series A, Mathematical, physical, and engineering sciences · 2019
    Article
  12. Article
  13. Uncertainty Quantification of a Multiscale Model for In-Stent Restenosis.Cardiovascular engineering and technology · 2018
    Article
  14. Article
  15. Article
  16. A cell-based mechanical model of coronary artery tunica media.Journal of the Royal Society, Interface · 2017
    Article
  17. Article
  18. Article
  19. Towards the virtual artery: a multiscale model for vascular physiology at the physics-chemistry-biology interface.Philosophical transactions. Series A, Mathematical, physical, and engineering sciences · 2016
    Article
  20. Magnetically enhanced cell delivery for accelerating recovery of the endothelium in injured arteries.Journal of controlled release : official journal of the Controlled Release Society · 2016
    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 at 1 institution in 1 country.

Hannan TahirComputational Science, Informatics Institute, Faculty of Science, University of Amsterdam, Amsterdam, The Netherlands. h.tahir@uva.nl
Carles Bona-Casas
Alfons G Hoekstra
University of Amsterdam · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Treatment of stenosed coronary arteries by balloon angioplasty and stenting results in arterial injury including severe damage to the endothelium at the site of treatment and initiates a complex cascade of inflammatory processes that may lead to the development of in-stent restenosis (ISR). Many clinical and biological factors involved in the progression of restenotic lesions have been studied in detail over the past few years but the mystery behind the pathophysiological mechanisms of this disease is still unresolved. In the present work, the effects of re-endothelialization and nitric oxide release on neointimal growth are investigated in-silico using a two dimensional multi-scale model of ISR. The effect of stent deployment depths on the development of ISR is studied as a function of time after stenting. Two dimensional domains were prepared by deploying bare metal stent struts at three different deployment depths into the tissue. Shear stress distribution on endothelial cells, obtained by blood flow simulations, was translated into nitric oxide production that keeps the smooth muscle cells in quiescent state. The cellular growth trends were plotted as a function of time and the data indicate a positive correlation between the neointimal growths and strut deployment depths in the presence of a functional endothelium, in qualitative agreement with in-vivo data. Additionally, no ISR is observed if a functional endothelium appears much earlier.

Indexed as

Models, BiologicalAngioplasty, Balloon, CoronaryAnimalsComputer SimulationCoronary CirculationCoronary RestenosisEndothelium, VascularHemodynamicsMyocytes, Smooth MuscleNeointimaNitritesPlatelet Endothelial Cell Adhesion Molecule-1Shear StrengthStentsSwineTime FactorsNitritesPlatelet Endothelial Cell Adhesion Molecule-1

Identifiers

PMID23785479
PMCPMC3681932
OpenAlexW2076787382

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.