Evidence map›Paper›PMID 33576407›Full record

ReviewCardiovascular research2021

Vascular smooth muscle cells in atherosclerosis: time for a re-assessment.

Mandy O J Grootaert, Martin R Bennett

Open access · greenAbstract readReview
In one paragraph

Review in Cardiovascular research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 308 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
308citing papers in PubMed, 2 pooled it
36.9field-weighted citation impact, top 1% 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

308 citing papers in PubMed, 2 syntheses or guidelines pooled it, 435 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Actin cytoskeletal dynamics in hepatic myofibroblasts and fibrosis.Nature reviews. Gastroenterology & hepatology · 2026
    Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. Olfactomedin 2 Promotes Atherosclerosis by Eliciting Smooth Muscle Foam Cell Formation.Arteriosclerosis, thrombosis, and vascular biology · 2026
    Article
  9. Olfactomedin-2 at the Crossroads of Smooth Muscle Cell Plasticity.Arteriosclerosis, thrombosis, and vascular biology · 2026
    Article
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  11. Article
  12. Review
  13. Article
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  16. Review
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  20. Article

248 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Mandy O J GrootaertDivision of Cardiovascular Medicine, University of Cambridge, Box 110, ACCI, Addenbrookes Hospital, CB2 0QQ Cambridge, UK.ORCID 0000-0003-1163-7499
Martin R BennettDivision of Cardiovascular Medicine, University of Cambridge, Box 110, ACCI, Addenbrookes Hospital, CB2 0QQ Cambridge, UK.ORCID 0000-0002-2565-1825
University of Cambridge · GB

Funding

British Heart Foundation CH/2000003/12800British Heart Foundation PG/16/11/32021British Heart Foundation PG/16/24/32090British Heart Foundation PG/16/63/32307British Heart Foundation RG/08/009/25841British Heart Foundation RG/13/14/30314British Heart Foundation RG/20/2/34763British Heart Foundation RG71070British Heart Foundation RG84554National Institute of Health Research Cambridge Biomedical Research Centre
6 · The paper itself

Abstract

Vascular smooth muscle cells (VSMCs) are key participants in both early and late-stage atherosclerosis. VSMCs invade the early atherosclerotic lesion from the media, expanding lesions, but also forming a protective fibrous cap rich in extracellular matrix to cover the 'necrotic' core. Hence, VSMCs have been viewed as plaque-stabilizing, and decreased VSMC plaque content-often measured by expression of contractile markers-associated with increased plaque vulnerability. However, the emergence of lineage-tracing and transcriptomic studies has demonstrated that VSMCs comprise a much larger proportion of atherosclerotic plaques than originally thought, demonstrate multiple different phenotypes in vivo, and have roles that might be detrimental. VSMCs down-regulate contractile markers during atherosclerosis whilst adopting alternative phenotypes, including macrophage-like, foam cell-like, osteochondrogenic-like, myofibroblast-like, and mesenchymal stem cell-like. VSMC phenotypic switching can be studied in tissue culture, but also now in the media, fibrous cap and deep-core region, and markedly affects plaque formation and markers of stability. In this review, we describe the different VSMC plaque phenotypes and their presumed cellular and paracrine functions, the regulatory mechanisms that control VSMC plasticity, and their impact on atherogenesis and plaque stability.

Indexed as

Cell PlasticityPlaque, AtheroscleroticAnimalsArteriesAtherosclerosisCell LineageHumansMuscle, Smooth, VascularMyocytes, Smooth MusclePhenotypeRupture, SpontaneousSignal TransductionAtherosclerosisVascular smooth muscle

Identifiers

PMID33576407
PMCPMC8479803
OpenAlexW3127304884

What Socratic 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 Socratic graph.