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. 2018 Jan 24;22(3):1366–1382. doi: 10.1111/jcmm.13462
• Introduction
• High‐cholesterol levels increase chemokine signalling
• Role of different monocyte subsets in atherosclerosis
• NR4A1‐deficient animal model
• Factors that associate impaired fat metabolism with the inflammatory responses in atherosclerosis
‐ Liver X receptors
‐ High cholesterol and hematopoietic progenitor cells
• The repertoire of hematopoietic progenitor cells is biased towards the preferential myeloid production in atherogenesis
• Mechanisms of monocyte release from the bone marrow
• Local macrophage proliferation is a major source of lesional macrophages
• Contribution of monocytes to plaque progression
• Factors that regulate macrophage retention or emigration from the plaque
• Neutrophils and their role in atherosclerosis
‐ Function and characteristics of neutrophils
‐ Components of neutrophil granules
‐ Neutrophilia and hypercholesterolaemia
‐ Mediators of neutrophil recruitment to lesions
‐Neutrophil granule components in atherosclerosis
‐ NETs in atherosclerosis
• Conclusion
• Acknowledgement
• Conflict of interest