,·维勒布兰德因子和血管衰老
Xia Wang1, Maria N Starodubtseva2,3, Carolyn M Kapron4
1Institute of Microvascular Medicine, The First Affiliated Hospital of Shandong First Medical University& Shandong Provincial Qianfoshan Hospital, Jinan, China.
npj aging
|June 1, 2023
概括
由内皮功能障碍驱动的血管衰老,因威尔布兰德因子 (vWF) 的升高而恶化. 低剂量暴露会增加vWF,造成心血管疾病和血管衰老的风险.
科学领域:
- 心血管科学 心血管科学
- 环境健康 环境健康
- 分子生物学分子生物学
背景情况:
- 血管衰老对心血管疾病有很大的贡献,心血管疾病的特征是血管变厚和变硬.
- 由氧化应激和炎症驱动的内皮细胞功能障碍是血管衰老的基础.
- 威尔布兰德因子 (vWF) 的血水平升高,这是一种参与凝血的糖蛋白,与衰老有关,并促进血栓形成和动脉样硬化.
研究的目的:
- 审查将vWF与血管衰老病理联系起来的分子机制.
- 为了检查 (Cd) 暴露如何影响vWF表达.
- 通过vWF升高提出低剂量的Cd作为血管衰老的风险因素.
主要方法:
- 关于分子机制的文献综述.
- 对血管衰老中的vWF研究的分析.
- 审查对对内皮细胞和vWF的影响的研究.
主要成果:
- 升高的vWF通过促进血栓形成,斑块形成和光滑肌肉细胞增殖,加剧了血管衰老.
- 低剂量暴露,在激活促生存途径的同时,增强了亲密介质厚度和动脉生成.
- 暴露会增加内皮细胞的vWF表达和分泌,无论是体内还是体外.
结论:
- vWF在与血管衰老相关的病理中发挥着关键作用.
- 低剂量的暴露会提高vWF水平.
- 低剂量暴露是血管衰老的潜在危险因素,通过增加的血vWF调解.
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