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在apoE/FXI双淘汰赛小鼠中的XI因子缺陷通过降低斑块内的MSR1mRNA表达来减少动脉样硬化
Reut Shnerb Ganor1,2, Elvezia M Paraboschi3,4, Duga Stefano3,4
1The Bert W. Strassburger Metabolic Center, Sheba Medical Center, Tel-Hashomer, Israel.
Journal of lipid and atherosclerosis
|October 6, 2025
概括
向凝血因子XI (FXI) 通过降低巨细胞清理受体1 (MSR1) 的调节,减少了小鼠的动脉样硬化. 这表明FXI是除了其抗血栓作用之外,也是动脉样硬化的潜在治疗点.
科学领域:
- 心血管研究研究心血管研究
- 分子生物学分子生物学
- 免疫学 免疫学 免疫学
背景情况:
- 动脉样硬化是全球主要的死亡原因,目前的治疗方法管理不充分.
- 在apolipoprotein E淘汰赛 (apoE-/-) 的小鼠中缺乏凝血因子XI (FXI) 会减少动脉样硬化.
- 通过FXI影响动脉样硬化的分子机制尚未完全理解.
研究的目的:
- 为了研究涉及到FXI介导动脉样硬化中的分子通路.
- 在动脉样硬化中识别受FXI缺失影响的特定基因和通路.
主要方法:
- 从apoE/FXI双淘汰赛 (DKO) 和apoE淘汰赛 (KO) 的小鼠身上捕获大动脉鼻斑块的激光微解剖.
- 斑块RNA的RNA测序和纳米链分析.
- 动脉样硬化病变的免疫组织化学分析.
主要成果:
- 在15353个基因中,64个基因在DKO和KO小鼠之间显示出显著的差异性表达.
- 基因组丰富分析显示,在apoE KO小鼠中,有8个高调节的代谢途径,其中7个与炎症有关.
- 与apoE KO小鼠相比,在DKO小鼠中观察到巨食者受体1 (MSR1) 的显著较低表达.
结论:
- 在apoE/FXI DKO小鼠下调的MSR1与减少动脉样硬化相关.
- 准FXI是一个潜在的抗动原原治疗策略.
- 抑制FXI可能会带来双重好处:抗血栓和抗动脉产生效应.
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