目的·利用单细胞RNA测序技术（single-cell?RNA?sequencing，scRNA-Seq）阐释冠状动脉粥样硬化（coronary atherosclerosis，CA）的细胞通信景观，挖掘主导细胞亚群及其关键基因。方法·下载GSE131778数据集并进行预处理、质控、降维聚类及注释；利用CellChat包进行细胞通信分析，识别主导细胞亚群。利用FindAllMarker函数，筛选主导细胞亚群与其他细胞亚群间的差异表达基因（differentially expressed genes，DEGs），并构建其蛋白相互作用（protein-protein interaction，PPI）网络，将Degree算法排序前五位的DEGs作为关键基因。将关键基因与CellChat分析出的细胞通信网络进行匹配和挖掘，获取关键基因参与的配体-受体对（ligand-receptor pair，L-R）及其介导的信号通路，并对结果进行可视化。构建动脉粥样硬化小鼠模型，并利用反转录聚合酶链式反应检测关键基因在颈动脉粥样硬化病变处的表达情况。结果·在CA病变处共鉴定出11个细胞亚群，包括平滑肌细胞、内皮细胞、巨噬细胞、单核细胞等。细胞通信分析结果显示，CellChat在11个细胞亚群中检测到70对显著的L-R和26条相关的信号通路；平滑肌细胞处于通信活跃状态，与其他细胞亚群间相互作用的次数和强度最显著，是主导细胞亚群。DEGs筛选结果显示，平滑肌细胞亚群和其他细胞亚群之间共有206个DEGs，其中ITGB2、PTPRC、CCL2、DCN、IGF1被识别为关键基因。关键基因介导的细胞通信分析结果显示：CCL2与ACKR1形成L-R，通过介导CCL信号通路参与平滑肌细胞与内皮细胞间的通信网络；ITGB2分别与ITGAM、ITGAX组成受体复合物，再与C3形成L-R介导补体信号通路，参与平滑肌细胞与巨噬细胞、单核细胞间的通信网络。动物实验对关键基因的验证结果同生物信息学分析的结果一致。结论·平滑肌细胞在CA病理过程中是主导细胞，与其他细胞间有广泛的通信网络，可通过CCL2-ACKR1、C3-（ITGAM+ITGB2）和C3-（ITGAX+ITGB2）介导的CCL和补体信号通路，与内皮细胞、巨噬细胞和单核细胞构建细胞通信网络。

Objective ·To use single-cell RNA sequencing (scRNA-Seq) technology to interpret the cellular communication landscape of coronary atherosclerosis (CA), and to explore the dominant cell subsets and their key genes. Methods ·The GSE131778 data set was downloaded and preprocessed, and quality controlling, dimension reduction clustering and annotation were carried out. Then cell communication analysis was conducted by using CellChat package to identify dominant cell subsets. The FindAllMarker function was used to screen differentially expressed genes (DEGs) between the dominant cell subpopulation and other cell subpopulations, and its protein-protein interaction (PPI) network was constructed. The DEGs ranked in the top five of the Degree algorithm were taken as key genes. Then, the key genes were matched and mined with the cell communication network analyzed by CellChat to obtain the ligand-receptor pairs (L-R) and the signal pathways mediated by the key genes, and the results were visualized. At the same time, the atherosclerosis mouse model was constructed and RT-PCR was used to detect the expression of key genes in carotid atherosclerosis lesions. Results ·A total of 11 cell subsets were identified in CA lesions, including smooth muscle cells, endothelial cells, macrophages, monocytes, etc. Cell communication results showed that CellChat detected 70 significant L-R and 26 related signal pathways in 11 cell subsets. Smooth muscle cell was the dominant cell subgroup with the most significant interaction frequency and intensity with other cell subgroups in the active state of communication. The results of DEGs screening showed that there were 206 DEGs between smooth muscle cell subsets and other cell subsets, among which ITGB2, PTPRC, CCL2, DCN and IGF1 were identified as key genes. The results of cell communication mediated by key genes showed that CCL2 and ACKR1 formed L-R and participated in the communication network between smooth muscle cells and endothelial cells through mediating CCL signaling pathway. ITGB2 formed receptor complexes withITGAM and ITGAX respectively, and then formed L-R with C3 to mediate the complement signal pathway, participating in the communication network among smooth muscle cells, macrophages and monocytes. The validation results of hub genes in animal experiments were consistent with the results of bioinformatics analysis. Conclusion ·Smooth muscle cells are the dominant cells in the pathological process of CA, and have extensive communication networks with other cells. They can construct cellular communication networks with endothelial cells, macrophages and monocytes through CCL and complement signaling pathways mediated by CCL2-ACKR1, C3-(ITGAM+ITGB2) and C3-(ITGAX+ITGB2).