Smooth muscle cells, endothelial cells and macrophages display remarkable heterogeneity within the healthy vasculature and under pathological conditions. During development, these cells arise from numerous embryological origins, which confound with different microenvironments to generate postnatal vascular cell diversity. In the atherosclerotic plaque milieu, all these cell types exhibit astonishing plasticity, generating a variety of plaque burdening or plaque stabilizing phenotypes. And yet how developmental origin influences intraplaque cell plasticity remains largely unexplored despite evidence suggesting this may be the case. Uncovering the diversity and plasticity of vascular cells is being revolutionized by unbiased single cell whole transcriptome analysis techniques that will likely continue to pave the way for therapeutic research. Cellular plasticity is only just emerging as a target for future therapeutics, and uncovering how intraplaque plasticity differs across vascular beds may provide key insights into why different plaques behave differently and may confer different risks of subsequent cardiovascular events.

平滑肌细胞、内皮细胞和巨噬细胞在健康脉管系统和病理条件下表现出显着的异质性。在发育过程中，这些细胞来自许多胚胎学起源，它们与不同的微环境混合，产生出生后血管细胞的多样性。在动脉粥样硬化斑块环境中，所有这些细胞类型都表现出惊人的可塑性，产生各种斑块负荷或斑块稳定表型。然而，尽管有证据表明情况可能如此，但发育起源如何影响斑块内细胞的可塑性仍然很大程度上未被探索。无偏见的单细胞全转录组分析技术正在彻底改变血管细胞多样性和可塑性的发现，这可能会继续为治疗研究铺平道路。细胞可塑性才刚刚成为未来治疗的目标，揭示不同血管床斑块内可塑性的差异可能会提供关键的见解，了解为什么不同斑块表现不同，并可能赋予后续心血管事件不同的风险。