Evidence map›Paper›PMID 29161303›Full record

ArticlePloS one2017

Nonlinear dynamics of early atherosclerotic plaque formation may determine the efficacy of high density lipoproteins (HDL) in plaque regression.

Alexander D Chalmers, Christina A Bursill, Mary R Myerscough

Abstract read
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In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing 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

13 citing papers in PubMed.

  1. Trial
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  9. An integrated approach to simulating the vulnerable atherosclerotic plaque.American journal of physiology. Heart and circulatory physiology · 2020
    Review
  10. Article
  11. Review
  12. International journal of molecular sciences · 2018
    Review
  13. 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.

Alexander D ChalmersSchool of Mathematics and Statistics, The University of Sydney, Sydney, NSW, Australia.
Christina A BursillSouth Australian Health and Medical Research Institute, Adelaide, South Australia, Australia.
Mary R MyerscoughSchool of Mathematics and Statistics, The University of Sydney, Sydney, NSW, Australia.ORCID http://orcid.org/0000-0002-4993-765X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We use a computational model to explore the effect of foam cell accumulation on plaque regression following an increase in high density lipoprotein (HDL) influx into the plaque. Atherosclerotic plaque formation is the outcome of cellular and cytokine responses to low density lipoproteins (LDL) that penetrate the artery wall following an injury to the endothelium and become modified. We modelled the cells and cytokines that are most important in plaque formation using partial differential equations. The model includes monocytes and macrophages, foam cells, macrophage chemoattractants, endothelium-stimulating cytokines, modified low density lipoproteins (mod LDL) and HDL. We included interactions both at the endothelium surface and inside the artery wall. The model predicts that when HDL influx into a well-established plaque with large numbers of foam cells is increased, the plaque may not regress but may continue to grow at a slower rate. If HDL influx is increased when a model plaque is recently established and has fewer foam cells, then the plaque does regress. If modLDL influx into the plaque is lowered at the same time that HDL influx increased or the capacity of the HDL to remove cholesterol from foam cells is increased, then the plaque is more likely to regress. The predictions of the model are in qualitative agreement with experimental studies in mice and rabbits. The results suggest that the intrinsic dynamics of reverse cholesterol transport by HDL are important in determining the success of HDL raising in promoting plaque regression.

Indexed as

Computer SimulationAnimalsArteriesAtherosclerosisCholesterolFoam CellsHumansLipoproteins, HDLLipoproteins, LDLMacrophagesMiceNonlinear DynamicsPlaque, AtheroscleroticRabbitsCholesterolLipoproteins, HDLLipoproteins, LDL

Identifiers

PMID29161303
PMCPMC5697811

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Registered trials

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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.