CLEC7A as a potential biomarker of atherosclerotic response to aspirin therapy: a multi-omics analysis

作者：Ke Cai, Dongjie Chen, Jingyu Wang, Jing Bai, Mengting Wang, Jianming Guo, Feng Liu, Jin‐Ao Duan, Shulan Su · 发表于：Frontiers in Immunology · 年份：2026 · DOI：10.3389/fimmu.2026.1727020 · 研究领域：Immune cells in cancer、Antiplatelet Therapy and Cardiovascular Diseases、Atherosclerosis and Cardiovascular Diseases

Many patients with atherosclerotic cardiovascular disease (ASCVD) do not respond well to aspirin therapy. This study employed a multi-omics approach to identify key genes associated with aspirin non-responsiveness, thereby providing potential molecular targets and theoretical basis for improving the precision treatment strategies for ASCVD patients. One aspirin non-responsiveness dataset and two atherosclerosis-related datasets were obtained from the Gene Expression Omnibus database. After identifying differentially expressed genes through weighted gene co-expression network analysis and differential expression analysis, we used machine learning techniques to screen for key genes and establish predictive models. The results showed that two key genes ( CLEC7A and RGS1 ) performed well in diagnosing aspirin non-responsiveness and ASCVD (area under the curve = 0.701–0.986). Among them, CLEC7A was significantly overexpressed in the aspirin non-responsiveness and ASCVD datasets ( P < 0.0001) and was identified as a potential risk factor. Furthermore, ELISA results showed overexpression of CLEC7A in the aortic tissue and serum of ASCVD mice ( P < 0.0001). In addition, immune infiltration analysis suggested that aspirin non-responsiveness mediated by CLEC7A may involve natural killer cells ( P = 0.04). However, CLEC7A-mediated ASCVD may involve regulatory T cells and neutrophils ( P < 0.0001), a finding further supported by immunofluorescence co-localization ana...