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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 \u2018necrotic\u2019 core. Hence, VSMCs have been viewed as plaque-stabilizing, and decreased VSMC plaque content\u2014often measured by expression of contractile markers\u2014associated 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.<\/jats:p>","DOI":"10.1093\/cvr\/cvab046","type":"journal-article","created":{"date-parts":[[2021,2,5]],"date-time":"2021-02-05T09:19:56Z","timestamp":1612516796000},"page":"2326-2339","source":"Crossref","is-referenced-by-count":509,"title":["Vascular smooth muscle cells in atherosclerosis: time for a re-assessment"],"prefix":"10.1093","volume":"117","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1163-7499","authenticated-orcid":false,"given":"Mandy O J","family":"Grootaert","sequence":"first","affiliation":[{"name":"Division of Cardiovascular Medicine, University of Cambridge, Box 110, ACCI, Addenbrookes Hospital, CB2 0QQ Cambridge, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2565-1825","authenticated-orcid":false,"given":"Martin R","family":"Bennett","sequence":"additional","affiliation":[{"name":"Division of Cardiovascular Medicine, University of Cambridge, Box 110, ACCI, Addenbrookes Hospital, CB2 0QQ Cambridge, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2021,2,8]]},"reference":[{"key":"2021092910121618800_cvab046-B1","doi-asserted-by":"crossref","first-page":"79","DOI":"10.1038\/nrcardio.2015.164","article-title":"Pathophysiology of native coronary, vein graft, and in-stent atherosclerosis","volume":"13","author":"Yahagi","year":"2016","journal-title":"Nat Rev Cardiol"},{"key":"2021092910121618800_cvab046-B2","doi-asserted-by":"crossref","first-page":"328","DOI":"10.1016\/j.arcmed.2015.06.006","article-title":"Global overview of the epidemiology of atherosclerotic cardiovascular 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