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内皮附录素A1的丧失加剧了由炎症引起的血管衰老

Qinyi You¹, Yilang Ke¹, Xiaofeng Chen¹

¹Department of Geriatrics, Fujian Medical University Union Hospital, Fujian Key Laboratory of Vascular Aging (Fujian Medical University), Fujian Institute of Geriatrics, Department of Cardiology, Fujian Heart Disease Center, Fujian Clinical Research Center for Vascular and Brain Aging, Fuzhou, Fujian, 350001, China.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)

|February 15, 2024

概括

附件A1 (ANXA1) 在防止血管衰老方面发挥着至关重要的作用. 失去ANXA1会加速衰老,而其补充或过度表达则可以防止炎症诱导的内皮细胞衰老和血管功能障碍.

科学领域:

心血管生物学心血管生物学
衰老研究研究衰老研究
炎症研究炎症研究

背景情况:

慢性炎症是血管衰老和与年龄有关的心血管疾病的关键驱动因素.
素A1 (ANXA1),一种抗炎因子,与年龄相关的疾病有关,但其在血管衰老中的作用尚不清楚.

研究的目的:

通过小鼠模型和细胞实验,研究ANXA1在血管衰老中的功能.
为了确定ANXA1是否能防止炎症诱导的内皮细胞衰老.

主要方法:

使用ANXA1淘汰 (ANXA1-/-) 和内皮细胞特异性ANXA1删除 (ANXA1△EC) 的小鼠模型.
使用的人类静脉内皮细胞 (HUVEC) 接受瘤亡因子-α (TNF-α) 诱导和ANXA1操纵 (敲击/过度表达).
评估了血管改造,功能障碍,细胞衰老标志物 (例如,β-银酸酶阳性,细胞循环停止),迁移和管道形成.

主要成果:

ANXA1 枯竭恶化了血管重塑和功能障碍,增加了与年龄和炎症相关的蛋白质表达.
补充Ac2-26,一个模仿ANXA1的,扭转了这些有害影响.
在HUVEC中抑制ANXA1促进了衰老,而在TNF-α诱导的衰老HUVEC中过度表达ANXA1减轻了衰老标志物并改善了细胞功能.
研究了甲基受体2 (FPR2) 在ANXA1介导的炎症反应中的作用.

结论:

与年龄相关的动脉炎症促进内皮细胞衰老,有助于血管衰老.
ANXA1通过抑制内皮细胞衰老和维持血管功能,作为抗血管衰老的保护因素.
向ANXA1或其通路可能提供治疗策略来延缓血管衰老和相关心血管疾病.

关键词:

附录A1 一,附录A1 一,附录A1 一.细胞内皮细胞的内皮细胞.炎症导致的炎症.血管衰老血管衰老

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