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Published on: December 19, 2014
Dietary compounds have potential in controlling atherosclerosis by modulating macrophage cholesterol metabolism and
Dongyan Shao1, Ziyang Lian1, Yichao Di1
11Key Laboratory for Space Bioscience and Biotechnology, School of Life Sciences, Northwestern Polytechnical University, 127 Youyi West Road, Xi'an, 710072 Shaanxi China.
Insights
Dietary compounds can inhibit atherosclerosis (AS) by targeting specific microRNAs (miRNAs) involved in cholesterol metabolism and inflammation. This review explores dietary compounds, miRNAs, and their roles in AS therapy.
Area of Science:
- Biomedical Science
- Cardiovascular Research
- Molecular Biology
Background:
- Atherosclerosis (AS) is a major cause of cardiovascular disease, initiated by cholesterol-laden macrophages in artery walls.
- Dysregulated cholesterol influx/efflux in macrophages and inflammation significantly promote AS development.
- MicroRNAs (miRNAs) play crucial roles in regulating macrophage cholesterol metabolism and inflammation in AS.
Purpose of the Study:
- To review current literature on dietary compounds targeting miRNAs for atherosclerosis (AS) therapy.
- To investigate the mechanisms by which dietary compounds influence macrophage cholesterol metabolism and inflammation via miRNAs.
- To identify challenges and guide future research in this therapeutic area.
Main Methods:
- Literature review of studies investigating dietary compounds, miRNAs, and atherosclerosis.
- Analysis of miRNA targets involved in cholesterol metabolism (e.g., ABCA1, ABCG1) and inflammation (e.g., NF-κB, Nrf2, PI3K/AKT pathways).
- Identification of specific miRNAs (e.g., miR-19b, miR-378, miR-10b, miR-33a/b, miR-155, miR-146a) modulated by dietary compounds.
Main Results:
- Dietary compounds inhibit AS by targeting miRNAs involved in cholesterol metabolism (miR-19b, miR-378, miR-10b, miR-33a/b) and inflammation (miR-155, miR-146a).
- While cholesterol-related miRNA targets vary among compounds, miR-155 is a common target in inflammation signaling.
- Key receptors (ABCA1, ABCG1) and signaling pathways (NF-κB, Nrf2, PI3K/AKT) are modulated by miRNAs in macrophages.
Conclusions:
- Dietary compounds offer a promising therapeutic strategy for atherosclerosis by modulating specific miRNA pathways.
- Targeting miRNAs involved in both cholesterol metabolism and inflammation presents a multifaceted approach to AS treatment.
- Further research is needed to overcome existing challenges and optimize dietary compound-mediated miRNA therapies for AS.
Abstract:
Atherosclerosis (AS) is a typical example of a widespread fatal cardiovascular disease. Accumulation of cholesterol-laden macrophages in the artery wall forms the starting point of AS. Increased influx of oxidized low-density lipoprotein to macrophages and decreased efflux of free cholesterol out of macrophages constitute major factors promoting the development of AS. Inflammation further aggravates the development of AS along or via interaction with the cholesterol metabolism. Many microRNAs (miRNAs) are related to the regulation of macrophage in AS in aspects of cholesterol metabolism and inflammation signaling. Dietary compounds perform AS inhibitory effects via miRNAs in the cholesterol metabolism (miR-19b, miR-378, miR-10b, miR-33a, and miR-33b) and two miRNAs in the inflammation signaling (miR-155 and miR-146a). The targeted miRNAs in the cholesterol metabolism vary greatly among different food compounds; however, in inflammation signaling, most food compounds target miR-155. Many receptors are involved in macrophages via miRNAs, including ABCA1 and ABCG1 as major receptors in the cholesterol metabolism, while nuclear factor-κB (NF-κB) and Nrf2 signaling and PI3K/AKT signaling pathways are targeted during inflammation. This article reviews current literature to investigate possible AS therapy with dietary compounds via targeting miRNAs. Currently existing problems were also discussed to guide further studies.
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