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用生物信息学识别心肌梗塞的诊断生物标志物,并使用针对异硫化的计算药物发现

Haoran Zhang¹, Ziguang Song², Weitao Shen³

¹Cardiovascular Medicine Ward, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.

Mediators of inflammation

|September 11, 2025

概括

这项研究确定了10个关键基因,这些基因与心肌梗塞 (MI) 中的二硫化症有关. 针对像MAP3K8和NFIL3这样的基因,通过提高细胞活力和减少细胞亡,显示出治疗心脏病的前景.

科学领域:

生物医学研究的研究.
计算生物学是一种计算生物学.
心血管科学心血管科学

背景情况:

失硫性脱硫症是一种新型受调细胞死亡机制,涉及各种疾病.
心肌梗塞 (MI) 是导致死亡的主要原因,需要新的治疗点.
了解MI的分子机制,包括细胞死亡途径,对于开发有效的治疗方法至关重要.

研究的目的:

通过计算来识别与心肌梗塞 (MI) 相关的与脱硫化相关的基因.
发现针对心脏病发作的新型诊断和治疗生物标志物.
探索已识别的基因在心脏病发作中的作用,并预测潜在的药物标.

主要方法:

差异基因表达分析 (limma) 和加权基因共表达网络分析 (WGCNA) 用于选候选基因.
生物标志物选择使用支持向量机-递归特征消除 (SVM-RFE) 和最小绝对收缩和选择操作员 (LASSO) 方法进行.
定量实时PCR (qRT-PCR),CCK-8测定,流细胞计和单细胞转录组分析 (Seurat,CellChat) 用于验证和机械洞察.

主要成果:

已经确定了10个与二硫症相关的基因 (THBD,IRAK3,NFIL3,IL1R2,THBS1,MAP3K8,JDP2,FCGR2A,CCL20,EREG) 是潜在的MI生物标志物.
在氧气-葡萄糖缺乏 (OGD) 诱导的细胞中观察到这些生物标志物的mRNA水平升高.
沉默MAP3K8和NFIL3改善了细胞活力,并减少了AC16-OGD细胞的亡,这表明它们在MI中发挥了关键作用.
免疫透分析表明,NFIL3和MAP3K8在MI的发病过程中影响T细胞功能.
单细胞分析揭示了MI中复杂的细胞-细胞通信网络,脂肪细胞作为中心枢纽.

结论:

已识别的10个基因代表了诊断和潜在治疗心肌梗塞的潜在新生物标志物.
MAP3K8和NFIL3是心脏病中细胞死亡和活力的关键调节者,是有前途的治疗点.
针对这些生物标志物可能为管理MI提供新的策略.
对已识别的细胞-细胞通信网络的进一步研究可能会揭示MI的额外治疗途径.

关键词:

生物标志物生物标志物硫化物脱硫症 (disulfidptosis) 是一种脱硫症.免疫调节免疫调节机器学习是机器学习.心肌梗塞的心脏病发作预测性药物预测性药物

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