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Updated: May 28, 2026
Quantitative Analysis of Cellular Composition in Advanced Atherosclerotic Lesions of Smooth Muscle Cell Lineage-Tracing Mice
Published on: February 20, 2019
Single-Cell Analysis, Spatial Transcriptomics and Molecular Docking Unveil Potential Therapeutic Targets for Carotid
Rongxing Qin1, Hongyu Xu2, Qingchun Qin1,3
1Department of Neurology, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region, China.
Background:
Carotid atherosclerosis (CAS) is a key cause of ischemic stroke that is strongly associated with increased risks of cardiovascular disease and vascular death, hence the urgent need to develop therapeutic strategies targeting carotid atherosclerotic plaques that would reduce the overall risk of cerebrovascular events.
Aims:
This study performs single-cell sequencing to dissect the cellular subpopulations in CAS. Molecular docking is used to uncover the potential therapeutic targets, consequently providing a theoretical basis for the CAS treatment strategies.
Study Design:
Integrated single-cell, spatial transcriptomic and molecular docking analysis.
Methods:
The single-cell sequencing data were retrieved from the Gene Expression Omnibus. Enrichment analyses were performed to characterize the cellular subpopulation functions. Accordingly, cell-cell communication networks were mapped to uncover the inter-subgroup interactions. Molecular docking was also employed to identify the potential therapeutic targets.
Results:
In this study, we identified the multiple cellular subpopulations that are associated with CAS. These CAS-related subpopulations engage in intercellular communication via distinct signaling pathways. Cannabidiol exhibits strong binding affinities for the macrophage, endothelial, and vascular smooth muscle cell markers. Spatial transcriptomics revealed that ACTC1, AKR1C2, and FABP4 exhibit region-specific expression patterns within the plaque.
Conclusion:
Dissecting the diverse cellular subpopulations in CAS and elucidating their functions and mechanisms, this study integrates single-cell sequencing, molecular docking, and spatial transcriptomics to offer fresh insights into CAS therapy.
Insights
Carotid atherosclerosis (CAS) involves diverse cell types communicating via signaling pathways. Cannabidiol shows potential therapeutic binding to key CAS cells, offering new treatment avenues.
Area of Science:
- Cardiovascular Research
- Genomics
- Pharmacology
Background:
- Carotid atherosclerosis (CAS) is a primary cause of ischemic stroke.
- CAS significantly increases risks for cardiovascular disease and vascular mortality.
- Developing targeted therapies for carotid atherosclerotic plaques is crucial to reduce cerebrovascular event risk.
Purpose of the Study:
- To dissect cellular subpopulations within carotid atherosclerosis (CAS) using single-cell sequencing.
- To identify potential therapeutic targets for CAS through molecular docking.
- To provide a theoretical foundation for novel CAS treatment strategies.
Main Methods:
- Integrated analysis of single-cell sequencing, spatial transcriptomics, and molecular docking.
- Retrieval and analysis of CAS single-cell sequencing data from Gene Expression Omnibus.
- Enrichment analyses, cell-cell communication network mapping, and molecular docking for target identification.
Main Results:
- Identification of multiple cellular subpopulations associated with CAS.
- Characterization of intercellular communication via distinct signaling pathways among CAS subpopulations.
- Cannabidiol demonstrated strong binding affinities for macrophage, endothelial, and vascular smooth muscle cell markers; spatial transcriptomics revealed region-specific expression of ACTC1, AKR1C2, and FABP4.
Conclusions:
- This study elucidates diverse cellular subpopulations in CAS and their functional mechanisms.
- Integration of single-cell sequencing, molecular docking, and spatial transcriptomics provides novel insights into CAS.
- Findings support the development of new therapeutic strategies targeting carotid atherosclerotic plaques.
