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大动脉化通过诱导心肌细胞的亡来加速心脏功能障碍

Nannan Hao¹, Hui Yong¹, Feifei Zhang¹

¹Department of Cardiology, the First Affiliated Hospital of Nanjing Medical University, China.

International journal of medical sciences

|January 3, 2024

概括

血管化通过增加动脉硬性和诱导心脏细胞亡来加速心脏功能障碍. 这项研究揭示了将化与心血管事件联系在一起的机制.

科学领域:

心血管生物学心血管生物学
病理生理学病理生理学
生物医学研究生物医学研究

背景情况:

血管化 (VC) 与心血管事件有关,但其机制尚不清楚.
动脉样硬化和慢性病与VC有关.
维生素和心脏功能障碍之间的确切关系需要进一步研究.

研究的目的:

调查链接血管化进展,动脉硬和心脏功能障碍的机制.
评估维生素D3诱导的血管化对小鼠心脏功能和亡的影响.
为了评估化血管光滑肌细胞对心肌细胞亡的直接影响,在体外.

主要方法:

给C57BL/6小鼠服用维生素D3,以诱导血管化.
评估了大动脉化,动脉弹性,脉冲波速度和心脏功能.
评估了心脏亡和基因表达,并将老鼠心肌细胞暴露在体外化的细胞介质中.

主要成果:

在小鼠中,维生素D3诱导了显著的大动脉化,增加了动脉硬性和心脏功能受损.
化大动脉表现出弹性溶解,心脏亡的增加,心脏基因表达的改变 (ANP,BNP,MMP2,bcl2/bax).
在体外,来自化血管光滑肌细胞的介质诱导了心肌细胞亡和改变了心脏基因表达.

结论:

血管化加速心脏功能障碍,部分是通过诱导心肌细胞亡.
静脉瘤的进展与动脉硬度增加和心脏功能受损有机联系.
这些发现凸显了VC作为心血管死亡率的关键因素.

关键词:

灭症 (apoptosis) 是一种死亡的过程.动脉硬性动脉硬性心脏功能障碍的心脏功能障碍血管化血管化维生素D3是维生素D3的重要组成部分.

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