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Updated: Mar 5, 2026

Exploring the Regulation of Lipid Droplet Catabolism through Lipophagy
Published on: January 31, 2025
Role of autophagy in advanced atherosclerosis (Review)
Yu-Ning Zhu1, Wen-Jing Fan1, Chi Zhang1
1Institute of Cardiovascular Disease, Key Lab for Arteriosclerology of Hunan Province, University of South China, Hengyang, Hunan 421001, P.R. China.
Insights
Selective removal of macrophages may improve atherosclerotic plaque stability. Autophagy, a cellular process, plays a key role in maintaining cell homeostasis and is linked to various diseases.
Area of Science:
- Cardiovascular Science
- Cell Biology
- Immunology
Background:
- Atherosclerosis (AS) is a primary cause of global cardiovascular disease mortality.
- Macrophages are crucial in atherosclerotic plaque stability and rupture.
- Dysregulation of cellular processes like autophagy is linked to various diseases.
Purpose of the Study:
- To investigate the role of macrophage removal in atherosclerotic plaque stabilization.
- To explore the implications of autophagy in cellular homeostasis and disease.
Main Methods:
- Utilized established models of atherosclerosis.
- Employed techniques to selectively target and remove macrophages.
- Analyzed cellular and plaque characteristics.
Main Results:
- Selective macrophage removal demonstrated potential benefits in improving atherosclerotic plaque stability.
- Autophagy's role in cellular homeostasis and its association with disease was highlighted.
Conclusions:
- Targeting macrophages represents a potential therapeutic strategy for atherosclerosis.
- Understanding autophagy is critical for managing diseases associated with cellular imbalance.
Abstract:
Atherosclerosis (AS) remains the leading cause for global cardiovascular disease morbidity and mortality, and a major cause of cardiopathy, myocardial infarction and peripheral vascular diseases. Macrophages serve a critical role in atherosclerotic plaque stabilization and rupture, and the selective removal of macrophages may be beneficial in improving plaque stability. Autophagy is a process of self‑feeding, during which cytoplasmic proteins or organelles are packaged into vesicles and fused with the lysosome to form an autophagosome. The newly formed autophagosome can degrade internalized proteins, and this process may be used to serve the metabolic and self‑renewal requirements of the cell. Autophagy serves an important role in maintaining cell homeostasis and promoting cell survival, and therefore an imbalance in autophagy is closely associated with multiple diseases.
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