Crosstalk Between Macrophages and Vascular Smooth Muscle Cells in Atherosclerotic Plaque Stability. Issue 4 (17th February 2022)

• Record Type: Journal Article
• Authors: Yurdagul, Arif
• Is Part Of: Arteriosclerosis, thrombosis, and vascular biology. Volume 42:Issue 4(2022)
• Page Start: 372
• Page End: 380
• Publication Date: 2022-02-17
• Subjects: atherosclerosis -- extracellular matrix -- lipoproteins -- macrophages -- muscle cells; Arteriosclerosis -- Periodicals; Thrombosis -- Periodicals; Blood-vessels -- Pathophysiology -- Periodicals; Electronic journals; 616.13
• DOI: 10.1161/ATVBAHA.121.316233
• Languages: English
• ISSNs: 1079-5642

Abstract

Abstract : Most acute cardiovascular events are due to plaque rupture, with atheromas containing large necrotic cores and thin fibrous caps being more susceptible to rupture and lesions with small necrotic cores and thick fibrous caps being more protected from rupture. Atherosclerotic plaques are comprised various extracellular matrix proteins, modified lipoprotein particles, and cells of different origins, that is, vascular cells and leukocytes. Although much has been revealed about the mechanisms that lead to plaque instability, several key areas remain incompletely understood. This In-Focus Review highlights processes related to cellular crosstalk and the role of the tissue microenvironment in determining cell function and plaque stability. Recent advances highlight critical underpinnings of atherosclerotic plaque vulnerability, particularly impairments in the ability of macrophages to clear dead cells and phenotypic switching of vascular smooth muscle cells. However, these processes do not occur in isolation, as crosstalk between macrophages and vascular smooth muscle cells and interactions with their surrounding microenvironment play a significant role in determining plaque stability. Understanding these aspects of cellular crosstalk within an atherosclerotic plaque may shed light on how to modify cell behavior and identify novel approaches to transform rupture-prone atheromas into stable lesions.