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

Cardiovascular research, 2021-09, Vol.117 (11), p.2326-2339 [Peer Reviewed Journal]

The Author(s) 2021. Published by Oxford University Press on behalf of the European Society of Cardiology. 2021 ;Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2021. For permissions, please email: journals.permissions@oup.com. ;Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2021. For permissions, please email: journals.permissions@oup.com. 2021 ;ISSN: 0008-6363 ;EISSN: 1755-3245 ;DOI: 10.1093/cvr/cvab046 ;PMID: 33576407

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  • Title:
    Vascular smooth muscle cells in atherosclerosis: time for a re-assessment
  • Author: Grootaert, Mandy O J ; Bennett, Martin R
  • Subjects: Animals ; Arteries - metabolism ; Arteries - pathology ; Atherosclerosis - genetics ; Atherosclerosis - metabolism ; Atherosclerosis - pathology ; Cell Lineage ; Cell Plasticity ; Humans ; Muscle, Smooth, Vascular - metabolism ; Muscle, Smooth, Vascular - pathology ; Myocytes, Smooth Muscle - metabolism ; Myocytes, Smooth Muscle - pathology ; Phenotype ; Plaque, Atherosclerotic ; Reviews ; Rupture, Spontaneous ; Signal Transduction
  • Is Part Of: Cardiovascular research, 2021-09, Vol.117 (11), p.2326-2339
  • Description: 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.
  • Publisher: England: Oxford University Press
  • Language: English
  • Identifier: ISSN: 0008-6363
    EISSN: 1755-3245
    DOI: 10.1093/cvr/cvab046
    PMID: 33576407
  • Source: Oxford Journals Open Access Collection
    GFMER Free Medical Journals
    MEDLINE
    Alma/SFX Local Collection

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