大动脉反会引起正常上升大动脉中的光滑肌细胞的表型调节
Brittany Balint1, Inés García Lascurain Bernstorff1, Tanja Schwab1
1Department of Thoracic and Cardiovascular Surgery, Saarland University Medical Center, Homburg/Saar, Germany.
The Journal of thoracic and cardiovascular surgery
|July 27, 2023
概括
大动脉反 (AR) 对大动脉光滑肌细胞 (SMC) 产生负面影响,改变其表型并促进衰老. 这些AR特异性变化发生在主动脉大小的独立性,但在双柱主动脉中更为严重.
科学领域:
- 心血管生物学 心血管生物学
- 大动脉疾病研究研究
- 血管细胞生物学 血管细胞生物学
背景情况:
- 大动脉反 (AR) 与上升的大动脉并发症有关.
- AR可能会对大动脉壁结构产生不利影响,即使没有扩张或有三管.
- 对大动脉光滑肌细胞 (SMC) 重建的AR的影响还不太清楚.
研究的目的:
- 研究AR患者上升性大动脉内SMC的变化.
- 确定AR是否影响SMC表型,包括收缩,合成和衰老.
- 探索大动脉形态在AR相关的SMC改变中的作用.
主要方法:
- 来自有正常门,大动脉狭窄 (AS) 或AR的患者的大动脉组织和中间SMC的分析.
- 对于SMC标记物 (阿尔法平滑肌动蛋白,维丁) 和衰老标记物 (p16INK4A,p21Cip1) 的免疫组织化学.
- 在体外培养SMC以评估复制能力和衰老.
主要成果:
- 与正常和AS相比,AR相关的大动脉组织显示α-平滑肌动蛋白减少,维丁,p16和p21增加.
- 与AR相关的SMCs表现出阿尔法平滑肌动蛋白减少,维丁增加和p16/p21表达的增加.
- 与AR相关的SMCs比AS大动脉的SMCs更早发生;影响在双大动脉上更为明显.
结论:
- 大动脉反直接损害了上升大动脉中的SMC表型.
- 这些AR特异性SMC变化独立于大动脉直径,但被双大动脉进一步加剧.
- 结果提供了关于AR相关的大动脉重塑和潜在治疗点的见解.
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