Evidence map›Paper›PMID 39653823›Full record

ReviewNature cardiovascular research2024

Chronic inflammation and vascular cell plasticity in atherosclerosis.

Alexander Lin, Joseph M Miano, Edward A Fisher, Ashish Misra

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature cardiovascular research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing 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

33 citing papers in PubMed.

  1. Trial
  2. Article
  3. Ilexoside K Ameliorates Atherosclerosis by Suppressing CD72Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  4. Olfactomedin-2 at the Crossroads of Smooth Muscle Cell Plasticity.Arteriosclerosis, thrombosis, and vascular biology · 2026
    Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. The theory of the inflammatory ecosystem.Science China. Life sciences · 2026
    Review
  13. Review
  14. Article
  15. Review
  16. Aqueous Extract ofNutrients · 2025
    Article
  17. Article
  18. Review
  19. Article
  20. 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

4 authors.

Alexander LinAtherosclerosis and Vascular Remodelling Group, Heart Research Institute, Sydney, New South Wales, Australia.
Joseph M MianoVascular Biology Center, Medical College of Georgia at Augusta University, Augusta, GA, USA.ORCID http://orcid.org/0000-0001-7522-3207
Edward A FisherDivision of Cardiology, Department of Medicine, New York University Grossman School of Medicine, New York, NY, USA.ORCID http://orcid.org/0000-0001-9802-143X
Ashish MisraAtherosclerosis and Vascular Remodelling Group, Heart Research Institute, Sydney, New South Wales, Australia. ashish.misra@hri.org.au.ORCID http://orcid.org/0000-0002-8901-4788

Funding

Molecular Regulation of Atherosclerosis Regression - RenewalR01HL084312 · NHLBI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI FISHER, EDWARD A · 2006 to 2024
$11.4M
National Heart Foundation of Australia (Heart Foundation) NHF1017U.S. Department of Health & Human Services | NIH | National Heart, Lung, and Blood Institute (NHLBI) R01HL084312
6 · The paper itself

Abstract

Vascular smooth muscle cells, endothelial cells and macrophages undergo phenotypic conversions throughout atherosclerosis progression, both as a consequence of chronic inflammation and as subsequent drivers of it. The inflammatory hypothesis of atherosclerosis has been catapulted to the forefront of cardiovascular research as clinical trials have shown that anti-inflammatory therapy reduces adverse cardiovascular events. However, no current therapies have been specifically designed to target the phenotype of plaque cells. Fate mapping has revealed that plaque cells convert to detrimental and beneficial cell phenotypes during atherosclerosis, with cumulative evidence highlighting that vascular cell plasticity is intimately linked with plaque inflammation, ultimately impacting lesion stability. Here we review vascular cell plasticity during atherosclerosis in the context of the chronic inflammatory plaque microenvironment. We highlight the need to better understand how plaque cells behave during therapeutic intervention. We then propose modulating plaque cell phenotype as an unexplored therapeutic paradigm in the clinical setting.

Indexed as

AtherosclerosisCell PlasticityInflammationPhenotypePlaque, AtheroscleroticAnimalsAnti-Inflammatory AgentsArteriesChronic DiseaseEndothelial CellsHumansInflammation MediatorsMacrophagesMuscle, Smooth, VascularMyocytes, Smooth MuscleSignal TransductionAnti-Inflammatory AgentsInflammation Mediators

Identifiers

What OpenQuestion holds

Textmetadata
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.