Abstract

Atherosclerosis is a chronic inflammatory disease characterized by the accumulation of lipids, smooth muscle cell proliferation, cell apoptosis, necrosis, fibrosis, and local inflammation. Immune and inflammatory responses have significant effects on every phase of atherosclerosis, and increasing evidence shows that immunity plays a more important role in atherosclerosis by tightly regulating its progression. Therefore, understanding the relationship between immune responses and the atherosclerotic microenvironment is extremely important. This article reviews existing knowledge regarding the pathogenesis of immune responses in the atherosclerotic microenvironment, and the immune mechanisms involved in atherosclerosis formation and activation.

Highlights

  • Atherosclerosis is a chronic inflammatory disease characterized by intense immunological activity

  • The formation of atherosclerotic plaques, which are characterized by the accumulation of lipids, local inflammation, smooth muscle cell (SMC) proliferation, cell apoptosis, necrosis, and fibrosis, is a major causative factor of arterial stenosis, and involves a chronic inflammatory response initiated by endothelial damage and inflammatory cell activation [2]

  • We presented research associated with the roles of inflammatory cells and cytokines in atherosclerotic plaque initiation and progression

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Summary

Introduction

Atherosclerosis is a chronic inflammatory disease characterized by intense immunological activity. Atherosclerosis can cause myocardial infarction and heart failure due to coronary artery stenosis, and in the brain, the stenosis or rupture of atherosclerotic plaques leads to transient ischemic attacks, ischemic stroke, or hemorrhage stroke. On other arterial branches of extremities, atherosclerosis can lead to peripheral arterial occlusion disease and critical limb ischemia. The formation of atherosclerotic plaques, which are characterized by the accumulation of lipids, local inflammation, smooth muscle cell (SMC) proliferation, cell apoptosis, necrosis, and fibrosis, is a major causative factor of arterial stenosis, and involves a chronic inflammatory response initiated by endothelial damage and inflammatory cell activation [2]. The atherosclerotic microenvironment and mechanisms associated with immune responses to atherosclerosis are discussed in detail

Roles of Lipid Metabolism in Atherosclerosis
LDL Modification and Oxidization in Atherosclerosis
Endothelial Function and Microenvironment
Role of ET-1 in Atherosclerosis
Roles of Immune-Mediator Regulation
Macrophages
Dendritic Cells
T Cells
Other Cells in Atherosclerosis
Plaque Rupture and Platelet Activation
Conclusions
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