Crosstalk Between Macrophages and Vascular Smooth Muscle Cells in Atherosclerotic Plaque Stability

被引:68
作者
Yurdagul, Arif, Jr. [1 ]
机构
[1] Louisiana State Univ Hlth Sci, Dept Mol & Cellular Physiol, Shreveport, LA 71130 USA
基金
美国国家卫生研究院;
关键词
atherosclerosis; extracellular matrix; lipoproteins; macrophages; muscle cells; GROWTH-FACTOR; EXTRACELLULAR-MATRIX; TRANSFORMING GROWTH-FACTOR-BETA-1; LIPID MEDIATORS; IN-VITRO; ACTIVATION; EXPRESSION; RECEPTOR; MODULATION; MYOCARDIN;
D O I
10.1161/ATVBAHA.121.316233
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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.
引用
收藏
页码:372 / 380
页数:9
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