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单细胞-内皮细胞相互作用作为克隆造血介导心血管疾病中的可向节点

Alyssa C Parker, J Brett Heimlich, Joseph C Van Amburg

medRxiv : the preprint server for health sciences

|September 15, 2025

概括

不确定潜力的克隆性血液形成 (CHIP) 改变单细胞-内皮细胞相互作用,有助于心血管疾病风险. 准CXCR2和ICAM1可能会恢复TET2CHIP患者的正常细胞相互作用.

科学领域:

心血管生物学心血管生物学
血液学血液学血液学
免疫学免疫学免疫学

背景情况:

不确定潜力的克隆性血液形成 (CHIP) 与心血管疾病 (CVD) 风险增加有关.
与CHIP相关的CVD背后的精确分子机制尚不清楚.
异常的单细胞-内皮细胞相互作用被假设为介导CHIP对心血管疾病的贡献.

研究的目的:

调查单细胞-内皮细胞相互作用在CHIP介导心血管疾病中的作用.
在CHIP中识别能够恢复正常单细胞内皮细胞功能的分子标.

主要方法:

单细胞RNA测序在CHIP患者 (TET2,DNMT3A) 和对照患者的单细胞和内皮细胞上进行.
预测了联体受体相互作用,并建立了单细胞-内皮细胞共同培养.
一个in silico扰动屏幕确定了潜在的治疗点,随后进行了体外实验验证.

主要成果:

基因基因基因基因基因基因基因基因基因基因基因基因基因基因基因基因基因基因基因基因基因基因基因基因基因基因基因基因基因基因基因基因基因基因基因基因基因基因基因基因基因基因
具有CHIP突变的单细胞在与内皮细胞相互作用时表现出降低的速度.
抑制ICAM1 (内皮细胞) 和CXCR2 (单细胞) 显著改善了TET2 CHIP单细胞的速度.

结论:

奇普基因突变会破坏正常的单细胞-内皮细胞相互作用.
准CXCR2和ICAM1是一个潜在的治疗策略,可以在TET2 CHIP中使这些相互作用正常化,从而有可能减轻心血管疾病风险.

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