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Updated: Jul 16, 2026
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Isolation and Profiling of Human Primary Mesenteric Arterial Endothelial Cells at the Transcriptome Level
Published on: March 14, 2022
Single-cell transcriptomics uncovers endothelial progenitor-like remodelling driving human coronary atherosclerosis
Fang Yao1,2, Fangzhou Li1,3, Shujie Gai1,3
1State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Nature Cell Biology
|July 14, 2026
Summary
Researchers mapped coronary atherosclerosis at a single-cell level, discovering a new endothelial cell (EC) subtype (EC5SLCO4A1+) that drives disease progression. Targeting PRDM15 may offer new therapies for atherosclerosis.
Area of Science:
- Cardiovascular Biology
- Cellular and Molecular Medicine
- Genomics and Transcriptomics
Background:
- Coronary atherosclerosis is a major cause of myocardial infarction and stroke.
- The cellular mechanisms driving atherosclerosis progression are not fully understood.
Purpose of the Study:
- To create a detailed cellular atlas of human coronary atherosclerosis.
- To identify novel cell states and molecular drivers of disease progression.
Main Methods:
- Single-cell RNA sequencing of 27,941 cells from 56 human coronary artery segments.
- Bioinformatic analysis to construct a disease-stage-resolved cellular atlas.
- In vivo studies using mouse models to investigate the role of PRDM15.
Main Results:
- Identified a progenitor-like endothelial cell (EC) subtype (EC5SLCO4A1+) that increases with atherosclerotic stage.
- Discovered PRDM15 drives the emergence of EC5SLCO4A1+ cells through transcriptional activation.
- Revealed extensive crosstalk between EC5SLCO4A1+ cells and immune cells, promoting disease progression.
- Demonstrated that endothelial PRDM15 overexpression exacerbates atherosclerosis, while suppression ameliorates it in vivo.
Conclusions:
- Endothelial cell subtype remodeling is central to human coronary atherosclerosis progression.
- The EC5SLCO4A1+ cell state and its driver PRDM15 represent potential therapeutic targets for atherosclerosis.
