Abstract
Atherosclerosis still is the primary cause of death worldwide. Our characterization of the atherosclerotic lesion is mainly rooted in definitions based on pathological descriptions. We often speak in absolutes regarding plaque phenotypes: vulnerable vs. stable plaques or plaque rupture vs. plaque erosion. By focusing on these concepts, we may have oversimplified the atherosclerotic disease and its mechanisms. The widely used definitions of pathology-based plaque phenotypes can be fine-tuned with observations made with various -omics techniques. Recent advancements in single-cell transcriptomics provide the opportunity to characterize the cellular composition of the atherosclerotic plaque. This additional layer of information facilitates the in-depth characterization of the atherosclerotic plaque. In this review, we discuss the impact that single-cell transcriptomics may exert on our current understanding of atherosclerosis.
Highlights
The classical concept of a “vulnerable plaque” originates from the 1980s and depicts plaque rupture in patients who died from coronary syndromes as the major pathological cause of acute myocardial infarction [1]
Genome-wide association studies (GWAS) and lesion-based transcriptomic studies point to a diverse landscape of mechanisms leading to atherosclerotic lesion initiation and progression
Fine-tuning the representation of the cellular composition and concomitant gene expression profiles is facilitated by single-cell RNA sequencing
Summary
The classical concept of a “vulnerable plaque” originates from the 1980s and depicts plaque rupture in patients who died from coronary syndromes as the major pathological cause of acute myocardial infarction [1]. We will discuss the current knowledge on cellular composition of lesions, lineage tracing experiments in mice, cell-cell communication, the importance of sex-stratified research, and examine the technical considerations of scRNA-seq research. For the future perspectives we examine spatial scRNAseq, the impact of scRNA-seq on pathological specification of atherosclerosis, cell plasticity, clonal expansion, integration of genetic and transcriptomic research, and the translation from mice to men.
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