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Updated: May 19, 2026

A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology
Published on: May 6, 2014
Novel immune signals and atherosclerosis
1Brigham and Women's Hospital, Department of Medicine, Cardiovascular Division, Center for Interdisciplinary Cardiovascular Sciences, 3 Blackfan Street, 17th Floor, Boston, MA 02115, USA. hiroiwata-circ@umin.ac.jp
Insights
Atherosclerosis, a chronic inflammatory process, involves immune signals and monocyte/macrophage biology. Understanding these mechanisms, including toll-like receptors (TLRs), is key to developing novel treatments for cardiovascular disease.
Area of Science:
- Cardiovascular Research
- Immunology
- Molecular Biology
Background:
- Atherosclerosis is the primary cause of coronary artery disease (CAD) and cerebrovascular disease, leading causes of mortality.
- Cardiovascular disease risk is reduced by controlling risk factors, notably lowering low-density lipoprotein (LDL) cholesterol with statins.
- Atherosclerosis is characterized as a chronic inflammatory condition initiated by risk factors, leading to endothelial dysfunction and inflammatory cell infiltration.
Purpose of the Study:
- To review the molecular mechanisms of immune signaling in atherosclerosis development and progression.
- To discuss the role of toll-like receptors (TLRs) in the pathogenesis of atherosclerosis.
- To explore monocyte/macrophage biology, including polarization and heterogeneity, in atherosclerosis progression.
Main Methods:
- Literature review summarizing current understanding of molecular mechanisms.
- Focus on immune signals, specifically toll-like receptors (TLRs).
- Analysis of monocyte/macrophage biology, including polarization and heterogeneity.
Main Results:
- Toll-like receptors (TLRs) are identified as potent inducers of inflammation and play a significant role in atherosclerosis pathogenesis.
- Monocyte and macrophage biology, encompassing polarization and heterogeneity, significantly contributes to atherosclerosis progression.
- Current knowledge highlights the interplay between molecular mechanisms and immune cell behavior in atherosclerosis.
Conclusions:
- Understanding the molecular mechanisms and immune cell orchestration is crucial for developing novel therapeutic strategies.
- Targeting immune pathways and monocyte/macrophage behavior offers potential for preventing and treating atherosclerosis.
- Further research into TLRs and macrophage dynamics can lead to innovative treatments for cardiovascular disorders.
Abstract:
Atherosclerosis underlies coronary artery disease (CAD) and cerebrovascular disease, which are the most common forms of life-threatening cardiovascular disorders. To minimize the risk of atherosclerotic complications, primary and secondary prevention strategies seek to control risk factors. Reducing low-density lipoprotein (LDL) cholesterol through lipid-lowering drugs, such as statins, in particular yields a proportional decrease in cardiovascular disease risk. Atherosclerosis is considered to be a complex chronic inflammatory process triggered by cardiovascular risk factors which cause endothelial dysfunction and inflammatory cell infiltration within the artery wall. In this review, we summarize the current understanding of the underling molecular mechanisms of the immune signals in the development and progression of atherosclerosis. Among various molecular mechanisms, toll like receptors (TLRs) are potent proinflammatory cytokines that operate to induce inflammation play an important role in the pathogenesis of atherosclerosis. Moreover, we discuss current knowledge regarding monocyte/macrophage biology that contributes to the progression of atherosclerosis, including macrophage polarization and heterogeneity. Understanding the molecular mechanisms in conjunction with orchestration of monocyte/macrophage biology should provide a basis for novel treatment strategies to prevent the development and progression of atherosclerosis.
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Atherosclerosis II: Clinical Manifestations and Diagnostic Tests
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