Aortic & peripheral vascular disease
Spatial transcriptomics reveals a key role of fibroblast-like vascular smooth muscle cells in human atherosclerotic cell crosstalk and stability
Authors' conclusion
This study provides the first comprehensive spatial transcriptomics map of cell communication in human plaque microenvironments. A pivotal role of a fibroblast-like VSMC, orchestrating intraplaque cell signalling and contributing to plaque stability, was identified.
Study context
- Population
- Human carotid atherosclerotic plaques13 carotid plaques
Methodological detailsspatial transcriptomics, single-cell transcriptomics, validation in apolipoprotein E (Apoe)-/- mice and in vitro, Single-cell transcriptomics (cells = 51 981), GWAS enrichment analyses; LINCS L1000 drug repurposing, Deconvolution of plaque bulk RNA-seq data (n = 78), histology and survival analyses
- Spatial transcriptomics
- Single-cell transcriptomics
- Validation in Apoe-/- mice and in vitro
- Single-cell transcriptomics (cells = 51 981)
- GWAS enrichment analyses; LINCS L1000 drug repurposing
- Deconvolution of plaque bulk RNA-seq data (n = 78), histology and survival analyses
Main finding
As reported in the abstract
- Fibroblast-like vascular smooth muscle cell (VSMC) phenotype (ECM formation pathways, validated in Apoe-/- mice) emerged as key regulator of intra-plaque ligand-receptor signalling, particularly in the cap region
- Higher proportion of fibroblast-like VSMCs in asymptomatics, associated with stable plaque features and predicted lower risk of future events
- Genes specific to this VSMC phenotype enriched in CAD and MI
- Compounds that could induce key marker genes identified and validated in vitro
Original publication
Spatial transcriptomics reveals a key role of fibroblast-like vascular smooth muscle cells in human atherosclerotic cell crosstalk and stability. Eur Heart J. Published 13 February 2026. doi:10.
Summarised from the published abstract; every number is checked against it