适应性免疫控制高血压中的区域大动脉重塑通过周血管脂肪组织可塑性
bioRxiv : the preprint server for biology
|August 8, 2025
概括
适应性免疫在高血压期间塑造大动脉重塑. T细胞促进胸前大动脉损伤,同时抑制保护性腹部适应,突出周围血管脂肪组织.
科学领域:
- 血管生物学和免疫学
- 心血管疾病病理生理学 病理生理学
- 脂肪组织生物学 脂肪组织生物学
背景情况:
- 高血压导致多种多样的大动脉重塑,区域机制不清楚.
- 适应性免疫在血管功能障碍和区域差异中的作用尚不清楚.
- 周血管脂肪组织 (PVAT) 越来越多地被认为对血管健康的影响.
研究的目的:
- 研究适应性免疫如何调节高血压条件下大动脉重塑的区域差异.
- 阐明T细胞和B细胞在调节PVAT表型和免疫代谢交叉反应中的作用.
- 确定PVAT作为高血压诱导的血管变化的潜在免疫代谢开关.
主要方法:
- 利用了安吉奥素II (AngII) 输注的野生型 (WT) 和Rag1小鼠 (缺乏T和B细胞).
- 集成的双轴机械测试,批量转录和PVAT分析.
- 评估了区域性大动脉重塑 (下降的胸前大动脉与下腹部大动脉) 和PVAT特征.
主要成果:
- WT小鼠表现出明显的胸前大动脉重塑与炎症;Rag1小鼠表现出减弱的变化,涉及T细胞.
- 在WT小鼠中,内腹主动脉表现出高血压性,但T细胞缺乏揭露了保护性代谢重编程.
- 胸部PVAT (T-PVAT) 在WT小鼠中变得有炎症作用,而Rag1小鼠的腹部PVAT (A-PVAT) 显示出热生成性可塑性.
结论:
- 适应性免疫,特别是T细胞,在高血压中决定了区域大动脉重塑模式.
- T细胞促进了不适应的胸前大动脉重塑,并抑制了保护性腹部适应.
- PVAT充当免疫代谢调节剂,影响区域血管敏感性,并为治疗干预提供点.
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