Vascular and Immune Cell Interactions in Atherosclerosis: Mechanisms, Plaque Destabilization, and Therapeutic Opportunities
- 1First Clinical College of Chinese Medicine, Hunan University of Chinese Medicine, Changsha 410208, China
- 2Hunan Key Laboratory of Colleges and Universities of Intelligent TCM Diagnosis and Preventive Treatment of Chronic Diseases, Hunan University of Chinese Medicine, Changsha 410208, China
- 3School of Chinese Medicine, Hunan University of Chinese Medicine, Changsha 410208, China
Abstract
Atherosclerosis (AS) is a progressive vascular disease characterized by lipid accumulation within the arterial intima, chronic inflammation, and plaque formation. It represents the underlying pathological basis of major cardiovascular and cerebrovascular events, including coronary artery disease, acute myocardial infarction, and ischemic stroke. Accumulating evidence suggests that the initiation and progression of AS are not driven by dysfunction of a single cell type but rather result from complex and dynamic interactions among multiple vascular resident and immune cells, including endothelial cells (ECs), vascular smooth muscle cells (VSMCs), macrophages, and lymphocytes. This review systematically summarizes the functional and phenotypic characteristics of these four major cell types in atherosclerotic lesions, with particular emphasis on their bidirectional regulatory networks. We provide an in-depth analysis of key intercellular communication mechanisms, including paracrine signaling, exosome-mediated transfer, oxidative stress crosstalk, and autophagy regulation, all of which play central roles in plaque microenvironment remodeling, lipid core expansion, fibrous cap degradation, and plaque destabilization. Furthermore, we highlight recent advances in translational strategies targeting cell–cell interactions, focusing on the mechanisms of action and clinical potential of representative agents.
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BibTeX
@article{zhou2026vascular,
title = {{Vascular and Immune Cell Interactions in Atherosclerosis: Mechanisms, Plaque Destabilization, and Therapeutic Opportunities}},
author = {Yingli Zhou and Keying Xiao and Yuhua Chen and Yixuan He and Yan Liu and Wenyu Zhang and Yuyi Zhang and Zhaoyang Dong and Zhihua Guo and Jinxia Li and Jiaming Wei},
journal = {Cells},
year = {2026},
month = oct,
doi = {10.3390/cells15211927},
url = {https://www.mdpi.com/2073-4409/15/21/1927},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Vascular and Immune Cell Interactions in Atherosclerosis: Mechanisms, Plaque Destabilization, and Therapeutic Opportunities
AU - Yingli Zhou
AU - Keying Xiao
AU - Yuhua Chen
AU - Yixuan He
AU - Yan Liu
AU - Wenyu Zhang
AU - Yuyi Zhang
AU - Zhaoyang Dong
AU - Zhihua Guo
AU - Jinxia Li
AU - Jiaming Wei
PY - 2026
DA - 2026/10/23
JO - Cells
DO - 10.3390/cells15211927
UR - https://www.mdpi.com/2073-4409/15/21/1927
AB - Atherosclerosis (AS) is a progressive vascular disease characterized by lipid accumulation within the arterial intima, chronic inflammation, and plaque formation. It represents the underlying pathological basis of major cardiovascular and cerebrovascular events, including coronary artery disease, acute myocardial infarction, and ischemic stroke. Accumulating evidence suggests that the initiation and progression of AS are not driven by dysfunction of a single cell type but rather result from complex and dynamic interactions among multiple vascular resident and immune cells, including endothelial cells (ECs), vascular smooth muscle cells (VSMCs), macrophages, and lymphocytes. This review systematically summarizes the functional and phenotypic characteristics of these four major cell types in atherosclerotic lesions, with particular emphasis on their bidirectional regulatory networks. We provide an in-depth analysis of key intercellular communication mechanisms, including paracrine signaling, exosome-mediated transfer, oxidative stress crosstalk, and autophagy regulation, all of which play central roles in plaque microenvironment remodeling, lipid core expansion, fibrous cap degradation, and plaque destabilization. Furthermore, we highlight recent advances in translational strategies targeting cell–cell interactions, focusing on the mechanisms of action and clinical potential of representative agents.
SN - 2073-4409
ER -