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HSPD1通过PPAR信号通路调节动脉素II诱导的心房动

Yimeng Zhou¹, Lianzhi Zhang¹, Shunping Zhou¹

¹Department of Cardiology, School of Medicine, Yangpu Hospital, Tongji University, Shanghai 200090, P.R. China.

Molecular medicine reports

|September 26, 2025

概括

热冲击蛋白D1 (HSPD1) 通过驱动心脏纤维细胞功能障碍,纤维化和炎症来促进心房动. 准HSPD1和PPAR通路为AF治疗提供了一个新的治疗策略.

科学领域:

心血管生物学心血管生物学
疾病的分子机制.
纤维化研究纤维化研究

背景情况:

心房动 (AF) 是一种复杂的疾病,需要对其分子基础有更深入的了解.
热冲击蛋白D1 (HSPD1) 已成为AF病变的潜在因素.
调查HSPD1在血管激素II (Ang II) 诱导的心脏纤维细胞 (CF) 中的作用对于向治疗的发展至关重要.

研究的目的:

阐明热冲击蛋白D1 (HSPD1) 在血管激素II (Ang II) 诱导的心脏纤维细胞 (CF) 激活中的作用及其对心房动 (AF) 发病因子的贡献.
通过对基因表达数据的生物信息学分析,识别参与AF的关键分子通路和蛋白质相互作用.
评估针对HSPD1和氧酶增殖器激活受体 (PPAR) 在AF中的信号传导的治疗潜力.

主要方法:

对GSE31821数据集的生物信息分析以识别差异表达基因 (DEG) 和构建蛋白质-蛋白质相互作用 (PPI) 网络,识别HSPD1作为枢纽基因.
使用 Ang II 治疗的心脏纤维细胞 (CF) 的体外实验,包括细胞活力试验,迁移试验,RT-qPCR,西式斑块和ELISA.
评估HSPD1对炎症性细胞因子,AF相关蛋白质和PPAR信号通路的淘汰效应,有或没有 thiazolidinedione 治疗.

主要成果:

生物信息分析确定了582个DEG,并突出了像MAPK和Wnt信号传递这样的途径,在AF样本中确定HSPD1为高度表达的基因.
ангиотензин II (Ang II) 诱导心脏纤维细胞 (CF) 的纤维变化,增加活力,迁移,纤维化标志物和HSPD1表达.
HSPD1 knockdown减弱了Ang II诱导的炎症和AF相关蛋白的表达,同时也影响了PPAR信号; thiazolidinedione部分逆转了Ang II的影响.

结论:

热冲击蛋白D1 (HSPD1) 在血管激素II (Ang II) 诱导的心脏纤维细胞 (CF) 功能障碍中发挥着关键作用,促进纤维化,炎症和AF相关蛋白质表达.
调节HSPD1活性和过氧体增殖器激活受体 (PPAR) 信号传导,为治疗心房 (AF) 提供了一个有前途的治疗途径.
针对HSPD1,可能与PPAR通路调节器结合,可以为AF管理提供一种新的策略.

关键词:

ангиотензин II 的使用心房动是心房动的一种.热冲击蛋白D1是一种热冲击蛋白D1.过氧体增殖器激活受体信号通路的信号通路.

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