Criminal Regulatory Approaches to Deepfake-Related Offenses: Focusing on the Crime of Fraud

Coronary artery disease (CAD), which is driven primarily by atherosclerosis, represents a major global health burden. This review explores the dynamic evolution of the CAD immune microenvironment through single-cell RNA sequencing (scRNA-seq), revealing cellular heterogeneity and interactions. On the basis of the American Heart Association’s histological classification of atherosclerotic lesions, we systematically summarize discoveries supported by scRNA-seq across disease stages (types I-V) from early monocyte recruitment and lipid-resistant macrophage subpopulations (e.g., CD52-hi macrophages) in initial lesions to intensified inflammation involving T-cell activation, NK cell differentiation, and macrophage polarization in fatty streaks and intermediate lesions and late-stage fibrosis and T-cell clonal expansion leading to plaque instability. Key findings highlight immune imbalance exacerbated by comorbidities such as diabetes and systemic lupus erythematosus (SLE), with potential biomarkers (e.g., JUN) and therapeutic targets (e.g., the CCL4‒CCR5 axis and SPP1+ macrophages). Methodological limitations, such as the lack of spatial information and challenges in inferring causal relationships, are discussed. Future prospects, such as spatial transcriptomics integration, multiomics approaches, and AI-assisted precision medicine, are also proposed. This review highlights the transformative role of scRNA-seq in advancing CAD pathology toward precision diagnostics and therapies.