识别和验证缺氧和代谢相关的枢纽基因和动脉样硬化中的细胞通信
Li Hao1, Qun Xu1, Guang Yang1
1Department of Gerontology, The First Affiliated Hospital of Shandong First Medical University & Shandong Provincial Qianfoshan Hospital, Jinan, Shandong, China.
Frontiers in cardiovascular medicine
|December 29, 2025
概括
这项研究确定了动脉样硬化 (AS) 中的关键代谢-低氧相关基因,揭示了这种复杂的血管疾病的新型诊断标记物和治疗点.
科学领域:
- 心血管生物学 心血管生物学
- 分子遗传学 分子遗传学
- 系统生物学 系统生物学
背景情况:
- 动脉样硬化 (AS) 是一种由斑块形成驱动的复杂疾病,其中细胞缺氧和新陈代谢改变至关重要.
- 在AS病变发生过程中,将新陈代谢和缺氧联系在一起的特定基因尚未得到很好的定义.
研究的目的:
- 在动脉样硬化中识别和表征差异表达的代谢-低氧相关基因 (DE-MH-RGs).
- 发现与这些基因相关的调节机制和潜在的诊断/治疗点.
主要方法:
- 对单细胞测序和AS相关数据集的分析.
- 与低氧相关的基因 (HRG) 和与代谢相关的基因 (MRG) 的交集以识别DE-MH-RG.
- 功能丰富 (GO,KEGG),蛋白与蛋白相互作用 (PPI) 网络建设,以及枢纽基因识别 (LASSO,GSEA,GSVA).
主要成果:
- 在AS中确定了五种细胞亚群:T淋巴细胞,内皮细胞,巨细胞,血管光滑肌细胞 (VSMC) 和B淋巴细胞.
- 与循环系统路径和缺氧反应相关的141个DE-MH-RGs的特征.
- 验证了五个具有诊断潜力的枢纽基因 (RYR2,ABCC9,KCNJ2,EGFR,SLC7A8),与代谢途径相关,主要位于VSMC中.
结论:
- 对AS的转录组分析揭示了关键的枢纽基因,这些基因连接了缺氧和新陈代谢.
- 这些发现为AS病原和潜在的治疗策略提供了宝贵的见解.
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