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作为急性心肌梗塞的预后标志物和治疗标的SP1的潜力:生物信息学,门德尔随机化和实验验证研究

Zhongyan Li¹, Huan Cheng¹, Jingru Li¹

¹Department of Cardiology, The First Affiliated Hospital of Kunming Medical University, Kunming, China.

Frontiers in immunology

|March 5, 2026

概括

这项研究确定SP1是急性心肌梗塞 (AMI) 铁死的一个关键因素. 建立了miR-133b/SP1/PLAUR途径作为AMI的潜在治疗标.

科学领域:

心血管生物学心血管生物学
分子医学是分子医学.
遗传学是一个遗传学.

背景情况:

急性心肌梗塞 (AMI) 是一个重大的全球健康挑战.
铁亡是一种受调节的细胞死亡途径,有助于AMI中的心肌细胞死亡.
与缺血损伤相关的特定铁亡相关基因 (FRG) 和分子途径在很大程度上仍未定义.

研究的目的:

为了确定关键的铁亡相关基因 (FRGs) 和急性心肌梗塞 (AMI) 相关的途径.
阐明 AMI 中铁的基础分子机制.
探索潜在的AMI诊断和治疗点.

主要方法:

在AMI数据集中对FRG的差异基因表达分析.
功能丰富分析 (GO/KEGG) 和蛋白质与蛋白质相互作用网络的构建.
基于总结数据的门德尔随机化 (SMR) 和贝叶斯同位化分析,以建立因果关系.
构建一个miRNA-TF-mRNA调节网络.
通过基因表达数据集的验证,转录因子结合部位的预测,GSEA,PheWAS和RT-qPCR.

主要成果:

在四个心血管组织中,SP1被确定为关键的转录因子,与AMI风险显著相关.
一个监管网络将miR-133b和PLAUR分别确定为关键miRNA和mRNA,形成miR-133b/SP1/PLAUR铁亡途径.
贝叶斯协同分析证实了SP1和AMI,以及PLAUR和AMI之间的强烈关系.
在MI中,miR-133b/SP1/PLAUR轴显示出作为预后标志物和治疗标的潜力.

结论:

通过综合转录组,SMR和PheWAS分析,确定了SP1和AMI风险之间的强有力的因果关系.
在AMI中,miR-133b/SP1/PLAUR铁亡途径被划定为关键机制.
已识别的途径及其组件代表了未来AMI诊断和治疗的有希望的目标.

关键词:

菲瓦斯 (Phewas) 是一种植物.SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 剧烈的心肌梗塞急性心肌梗塞生物信息学是一种生物信息学.定位化分析分析的分析.铁性化 (ferroptosis) 是一种这是一个miRNA-TF-mRNA网络.基于总结数据的MR总结数据

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