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The involvement of MCs in the pathology of atherosclerosis is supported by their accumulation in atherosclerotic plaques upon their progression and the association of intraplaque MC numbers with acute cardiovascular events. MCs that accumulate within the atherosclerotic plaque release a cocktail of mediators through which they contribute to neovascularization, plaque progression, instability, erosion, rupture, and thrombosis. At a molecular level, MC-released proteases, especially cathepsin G, degrade low-density lipoproteins (LDL) and mediate LDL fusion and binding of LDL to proteoglycans (PGs). Through a complicated network of chemokines including CXCL1, MCs promote the recruitment of among others CXCR2<jats:sup>+<\/jats:sup> neutrophils, therefore, aggravating the inflammation of the plaque environment. Additionally, MCs produce extracellular traps which worsen inflammation and contribute to atherothrombosis. Altogether, evidence suggests that MCs actively, via several underlying mechanisms, contribute to atherosclerotic plaque destabilization and acute cardiovascular syndromes, thus, making the study of interventions to modulate MC activation an interesting target for cardiovascular medicine.<\/jats:p>","DOI":"10.1007\/s12016-024-08981-9","type":"journal-article","created":{"date-parts":[[2024,1,30]],"date-time":"2024-01-30T14:02:52Z","timestamp":1706623372000},"page":"30-49","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":32,"title":["Cellular and Molecular Mechanisms of Mast Cells in Atherosclerotic Plaque Progression and Destabilization"],"prefix":"10.1007","volume":"66","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0546-5280","authenticated-orcid":false,"given":"Daniel","family":"Elieh-Ali-Komi","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1242-1959","authenticated-orcid":false,"given":"Ilze","family":"Bot","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9149-1137","authenticated-orcid":false,"given":"M\u00f3nica","family":"Rodr\u00edguez-Gonz\u00e1lez","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4121-481X","authenticated-orcid":false,"given":"Marcus","family":"Maurer","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2024,1,30]]},"reference":[{"issue":"7","key":"8981_CR1","doi-asserted-by":"publisher","first-page":"1524","DOI":"10.1016\/j.ajpath.2018.03.011","volume":"188","author":"M Zuiderwijk","year":"2018","unstructured":"Zuiderwijk M et al (2018) Leukocyte dynamics during the evolution of human coronary atherosclerosis: conclusions from a sevenfold, chromogen-based, immunohistochemical evaluation. 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