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Nutraceuticals for prevention of atherosclerosis: Targeting monocyte infiltration to the vascular endothelium

保健品 单核细胞 炎症 医学 内皮 免疫学 癌症研究 病理 内科学
作者
Min Jeong Kim,Sung Keun Jung
出处
期刊:Journal of Food Biochemistry [Wiley]
卷期号:44 (6) 被引量:12
标识
DOI:10.1111/jfbc.13200
摘要

Cardiovascular disease (CVD) is the leading cause of death, globally, and is a serious problem in developing countries. Preventing atherosclerosis is key to reducing the risk of developing CVD. Similar to carcinogenesis, atherogenesis can be divided into four stages: initiation, promotion, progression, and acute events. The current study focuses on the promotion stage, which is characterized by circular monocyte penetration into vascular endothelial cells, monocyte differentiation into macrophages, and the formation of foam cells. This early stage of atherogenesis is a major target for nutraceuticals. We discuss nutraceuticals that can potentially inhibit monocyte adhesion to the vascular endothelium, thereby preventing the promotional stage of atherosclerosis. The mechanisms through which these nutraceuticals prevent monocyte adhesion are classified according to the following targets: NF-κB, ROS, MAPKs, and AP-1. Additionally, we discuss promising targets for nutraceuticals that can regulate monocyte adhesion to the endothelium. Practical applications Introduction of atherogenesis with initiation, promotion, progression, and acute events provide specific information and factors for each step in the development of atherosclerosis. Functional food or pharmaceutical researchers can set target stages and use them to develop materials that control atherosclerosis. In particular, because it focuses on vascular inflammation via interaction between monocytes and vascular endothelial cells, it provides specific information to researchers developing functional foods that regulate this process. Therefore, this manuscript, unlike previous papers, will provide material information and potential mechanisms of action to researchers who want to develop functional foods that control vascular inflammation rather than vascular lipids.
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