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Updated: Jul 11, 2025
Isolation of Endothelial Cells from the Lumen of Mouse Carotid Arteries for Single-Cell Multi-Omics Experiments
Published on: October 4, 2021
Integrative single-cell meta-analysis reveals disease-relevant vascular cell states and markers in human
Jose Verdezoto Mosquera1, Gaëlle Auguste2, Doris Wong1
1Department of Biochemistry and Molecular Genetics, University of Virginia, Charlottesville, VA 22908, USA; Center for Public Health Genomics, University of Virginia, Charlottesville, VA 22908, USA.
Insights
This study maps human atherosclerosis using single-cell data, revealing modulated smooth muscle cells (SMCs) are key in coronary artery disease (CAD). New markers identify disease progression, aiding cardiovascular disease research.
Area of Science:
- Cardiovascular Biology
- Genomics
- Immunology
Background:
- Coronary artery disease (CAD) involves plaque buildup driven by cellular interactions.
- Understanding human cell phenotypes in atherosclerosis is crucial but challenging.
- Single-cell RNA sequencing (scRNA-seq) offers detailed cellular insights.
Conclusions:
- The developed atlas provides a unified view of human atherosclerosis.
- Modulated SMCs are a significant factor in CAD pathogenesis.
- Identified markers offer potential for mechanistic and translational cardiovascular disease studies.
Abstract:
Coronary artery disease (CAD) is characterized by atherosclerotic plaque formation in the arterial wall. CAD progression involves complex interactions and phenotypic plasticity among vascular and immune cell lineages. Single-cell RNA-seq (scRNA-seq) studies have highlighted lineage-specific transcriptomic signatures, but human cell phenotypes remain controversial. Here, we perform an integrated meta-analysis of 22 scRNA-seq libraries to generate a comprehensive map of human atherosclerosis with 118,578 cells. Besides characterizing granular cell-type diversity and communication, we leverage this atlas to provide insights into smooth muscle cell (SMC) modulation. We integrate genome-wide association study data and uncover a critical role for modulated SMC phenotypes in CAD, myocardial infarction, and coronary calcification. Finally, we identify fibromyocyte/fibrochondrogenic SMC markers (LTBP1 and CRTAC1) as proxies of atherosclerosis progression and validate these through omics and spatial imaging analyses. Altogether, we create a unified atlas of human atherosclerosis informing cell state-specific mechanistic and translational studies of cardiovascular diseases.
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