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Quantitative Analysis of Cellular Composition in Advanced Atherosclerotic Lesions of Smooth Muscle Cell Lineage-Tracing Mice
Published on: February 20, 2019
Multifaceted cell death in atherosclerosis: Mechanisms, pathological impact, and therapeutic targeting
Wang-Jing Mu1, Shi-Qi Wei1, Wan-Qiu Peng2
1Key Laboratory of Exercise and Health Sciences of the Ministry of Education, Shanghai University of Sport, Shanghai 200438, China; School of Exercise and Health and Collaborative Innovation Center for Sports and Public Health, Shanghai University of Sport, Shanghai 200438, China; Shanghai Key Lab of Human Performance, Shanghai University of Sport, Shanghai 200438, China; Shanghai Frontiers Science Research Base of Exercise and Metabolic Health, Shanghai University of Sport, Shanghai 200438, China.
Abstract:
Atherosclerosis (AS) is a chronic inflammatory vascular disease associated with aging, the initiation and progression of which is closely related to multiple cell death pathways. This review systematically elucidates the specific activation mechanisms and pathological contributions of ferroptosis, pyroptosis, apoptosis, autophagic cell death, necroptosis, NETosis, cuproptosis, parthanatos, and PANoptosis in vascular endothelial cells (VECs), macrophages, vascular smooth muscle cells (VSMCs), and neutrophils. Collectively, they drive core plaque necrosis, thinning of the fibrous cap, exacerbated inflammation, and thrombosis, ultimately precipitating acute clinical cardiovascular and cerebrovascular events. In addition, therapeutic strategies targeting these pathways are summarized. In-depth understanding of the effects and mechanisms of different forms of cell death in different types of cells would open doors to developing safe and effective interventions against AS. In summary, the progression of AS is driven by the parallel or sequential activation of multiple programmed cell death pathways in different vascular cells; systematically targeting these pathways holds promise as a new strategy to stabilize plaques and prevent acute events.
Insights
Atherosclerosis progression involves multiple cell death pathways like ferroptosis and pyroptosis in vascular cells. Targeting these programmed cell death mechanisms offers a promising strategy for plaque stabilization and preventing cardiovascular events.
Area of Science:
- Cardiovascular Research
- Cell Biology
- Immunology
Background:
- Atherosclerosis (AS) is a chronic inflammatory vascular disease linked to aging.
- Multiple programmed cell death pathways are implicated in AS initiation and progression.
Purpose of the Study:
- To systematically review cell death mechanisms in Atherosclerosis.
- To elucidate the pathological roles of various cell death pathways in vascular cells.
Main Methods:
- Systematic review of literature on programmed cell death in Atherosclerosis.
- Analysis of mechanisms of ferroptosis, pyroptosis, apoptosis, and other cell death forms.
- Examination of cell death contributions in vascular endothelial cells, macrophages, VSMCs, and neutrophils.
Main Results:
- Multiple cell death pathways (ferroptosis, pyroptosis, apoptosis, etc.) are activated in different vascular cells during AS.
- These pathways contribute to plaque necrosis, fibrous cap thinning, inflammation, and thrombosis.
- Activation of these pathways precipitates cardiovascular and cerebrovascular events.
Conclusions:
- AS progression is driven by parallel/sequential activation of multiple programmed cell death pathways.
- Targeting these diverse cell death pathways presents a novel therapeutic strategy for AS.
- Understanding cell death mechanisms in specific vascular cells is key to developing effective AS interventions.
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