在冠状动脉疾病患者中,PCSK9和冠状动脉样硬化的进展超过了LDL胆固醇
Rosetta Ragusa1, Silvia Rocchiccioli1, Serena Del Turco1
1CNR, Institute of Clinical Physiology, Pisa, Italy.
European journal of clinical investigation
|June 4, 2025
概括
血PCSK9水平与冠状动脉疾病 (CAD) 斑块进展相关,特别是死核. 这表明PCSK9可能通过超出LDL-C的炎症途径促进不良斑块表型.
科学领域:
- 心血管研究研究心血管研究
- 动脉样硬化生物学 动脉样硬化生物学
- 分子医学是分子医学.
背景情况:
- 冠状动脉疾病 (CAD) 仍然是全球死亡的主要原因.
- 了解推动动脉样硬化进展的分子机制对于开发新疗法至关重要.
- 血性蛋白转化酶亚提利辛/凯辛9型 (PCSK9) 是LDL胆固醇代谢的关键调节者.
研究的目的:
- 为了研究血PCSK9水平和冠状动脉斑块进展在患有CAD的患者之间的联系.
- 探索可能将PCSK9与动脉生成联系起来的分子途径.
主要方法:
- 159名患有稳定的CAD的患者在基线和平均6.5年的随访后接受了冠状动脉计算机断层扫描血管造影 (CTA).
- 斑块的进展是通过斑块体积的年度变化来量化 (总体,纤维,纤维脂肪,死核,密).
- 为了分析PCSK9相关途径,进行了全血和体外内皮细胞 (EC) 研究的RNA测序.
主要成果:
- 较高的血PCSK9水平显着与核斑块体积的年均进展增加相关 (p=0.022),独立于传统的危险因素和降脂疗法.
- RNA测序显示,PCSK9的表达与参与天生的免疫反应的基因有关.
- 实验室研究表明,PCSK9治疗显著上调了内皮细胞中的炎症标志物 (ICAM-1,VCAM-1,MCP1,IL6).
结论:
- 血PCSK9是冠状动脉斑块进展的独立预测因子,特别是易受伤害的死核组成部分,在患有CAD的患者中.
- 通过炎症机制,PCSK9可能会通过其在LDL-C调节中的作用来促进预后不利的斑块表型的发展,这是独立于其在LDL-C调节中的作用.
- 这些发现凸显了PCSK9作为稳定动脉样硬化斑块的潜在治疗点.
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