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Published on: October 17, 2017
Mitochondrial Omics in Macrophage Foam Cell Formation and Atherosclerosis
Enhui Wu1,2, Zengyu Wang2, Yiwen Wang2
1Department of Thoracic Surgery, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, China.
Insights
Mitochondrial dysfunction in macrophages drives atherosclerosis by promoting foam cell formation and plaque inflammation. Targeting mitochondrial metabolism offers a strategy to combat cardiovascular disease progression.
Area of Science:
- Cardiovascular Biology
- Cellular Metabolism
- Immunology
Background:
- Atherosclerotic cardiovascular disease (ASCVD) is a major global health concern.
- Macrophages are key players in atherosclerosis, forming foam cells that drive plaque development.
- Mitochondrial metabolism significantly influences macrophage function in atherosclerosis.
Purpose of the Study:
- To review macrophage heterogeneity and foam cell formation in atherosclerotic plaques.
- To compare various mitochondrial omics approaches for studying atherosclerosis.
- To discuss the role of mitochondrial dysfunction in macrophage-driven atherosclerosis.
Main Methods:
- Review of high-throughput omics technologies (proteomics, metabolomics, lipidomics, etc.).
- Comparison of traditional and emerging omics strategies (single-cell, spatial omics).
- Analysis of bioinformatic methods for mitochondrial function investigation.
Main Results:
- Macrophages exhibit heterogeneity within atherosclerotic plaques.
- Mitochondrial dysfunction and metabolic reprogramming contribute to foam cell formation.
- Altered mitochondrial function exacerbates plaque inflammation and instability.
Conclusions:
- Mitochondrial metabolism is a critical target for therapeutic intervention in atherosclerosis.
- Advanced omics technologies provide deep insights into macrophage mitochondrial biology.
- Understanding mitochondrial roles in macrophages can lead to improved ASCVD treatments.
Abstract:
Atherosclerotic cardiovascular disease (ASCVD) is a leading cause of death worldwide, with atherosclerosis serving as the core pathological mechanism driving ischemic heart disease, ischemic stroke, and peripheral artery disease. Macrophages play a central role in atherosclerosis by internalizing modified lipids and transforming them into foam cells, thereby driving plaque formation and progression. Mitochondrial metabolism is critically involved in regulating macrophage function, and targeting mitochondrial dysfunction may provide strategies for limiting plaque inflammation and improving plaque stability. Advances in high-throughput omics technologies and bioinformatic analysis methods have provided powerful tools for in-depth investigation of mitochondrial function. This review first summarizes macrophage heterogeneity and foam cell formation in atherosclerotic plaques. It then compares mitochondrial omics approaches, including proteomics, interactomics, metabolomics, lipidomics, isotope tracing, and emerging single-cell and spatial omics strategies. Finally, it discusses how mitochondrial dysfunction and metabolic reprogramming contribute to macrophage foam cell formation, plaque inflammation, and atherosclerosis progression.
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