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Updated: Jan 8, 2026
Quantitative Analysis of Cellular Composition in Advanced Atherosclerotic Lesions of Smooth Muscle Cell Lineage-Tracing Mice
Published on: February 20, 2019
Investigation for atherosclerotic plaque rupture with thrombosis in mice based on single-cell sequencing and
Peng Nie1, Fang Wan1, Tianbao Yao1
1Division of Cardiology, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Introduction:
Atherosclerotic plaque rupture with thrombus formation leads to severe cardiovascular events. We hoped to explore the hub genes providing critical roles in the process of atherosclerotic plaque rupture accompanied by thrombus formation, which might provide a new research direction for clinical therapy.
Methods:
The mouse model of atherosclerotic plaque rupture with thrombosis was established by the combined ligation of the left renal artery and common carotid artery, while key genes and regulatory pathways were identified using single-cell RNA sequencing and bioinformatics analysis.
Results:
The mice model accompanied by atherosclerotic plaque rupture with thrombus formation was successfully established. Seventeen cell subsets were identified based on scRNA-seq analysis including Fibroblasts. Downstream analysis showed 376 TDEGs were revealed to be closed associated with thrombosis-prone plaques. These TDEGs were mainly enriched in cell adhesion. A total of five hub genes including COL5A1, VCAN, PTGS2, ITGAV, and ITGA8 were investigated. Drug-gene interaction network analysis identified several drug-gene relations, such as Aspirin-PTGS2. Fibroblasts might play a vital role in atherosclerotic plaque rupture with thrombosis.
Discussion:
COL5A1, VCAN, PTGS2, ITGAV and ITGA8 might be novel biomarkers for atherosclerotic plaque rupture with thrombosis. ITGAV and VCAN might take part in the process atherosclerotic plaque rupture with thrombosis via cell adhesion function.
Insights
Atherosclerotic plaque rupture and thrombosis are linked to cardiovascular events. Five hub genes (COL5A1, VCAN, PTGS2, ITGAV, ITGA8) were identified as potential biomarkers for this process.
Area of Science:
- Cardiovascular Biology
- Genomics
- Thrombosis Research
Background:
- Atherosclerotic plaque rupture leading to thrombus formation is a major cause of cardiovascular events.
- Identifying key molecular players in this process is crucial for developing new therapeutic strategies.
Purpose of the Study:
- To explore hub genes critical in atherosclerotic plaque rupture with thrombus formation.
- To identify potential biomarkers and therapeutic targets for cardiovascular events.
Main Methods:
- Establishment of a mouse model for atherosclerotic plaque rupture with thrombosis.
- Single-cell RNA sequencing (scRNA-seq) and bioinformatics analysis to identify key genes and pathways.
- Drug-gene interaction network analysis.
Main Results:
- Successfully established a mouse model of atherosclerotic plaque rupture with thrombosis.
- Identified 17 cell subsets, including fibroblasts, and 376 differentially expressed genes (TDEGs) associated with thrombosis-prone plaques.
- Discovered five hub genes: COL5A1, VCAN, PTGS2, ITGAV, and ITGA8, enriched in cell adhesion pathways.
- Found potential drug-gene interactions, e.g., Aspirin-PTGS2.
Conclusions:
- COL5A1, VCAN, PTGS2, ITGAV, and ITGA8 may serve as novel biomarkers for atherosclerotic plaque rupture and thrombosis.
- ITGAV and VCAN may contribute to plaque rupture and thrombosis through cell adhesion mechanisms.
- Fibroblasts are suggested to play a significant role in atherosclerotic plaque rupture with thrombosis.
