陈淼然,郭可欣,贺忠梅,宁俊娅,封启龙,高丽娟,曹济民

• 1:山西医科大学第二临床医学院
• 2:山西医科大学细胞生理学教育部重点实验室细胞生理学山西省重点实验室生理学系

摘要(Abstract)：

目的 分析心力衰竭潜在的相关基因以及相关机制。方法 从基因表达综合数据库中下载数据集GSE18703，使用R软件中“limma”包分析差异表达基因（DEGs）。对DEGs进行基因本体论（GO）和京都基因和基因组百科全书（KEGG）通路富集分析，以探索心力衰竭相关的生物学功能和信号通路。使用Cytoscape软件构建蛋白质相互作用（PPI）网络，识别心力衰竭发病机制相关的关键基因，用荧光定量聚合酶链反应（qPCR）法对血管紧张素Ⅱ（AngⅡ）诱导的大鼠H9C2心肌细胞模型进行转录水平的验证。通过h TFtarget数据库分析关键基因的转录因子网络，以探究心力衰竭的发生机制。结果 共筛选出292个DEGs，其中上调基因140个，下调基因152个。GO分析显示，DEGs主要富集于细胞外区、细胞外空间、血液微粒等细胞成分以及嗅觉转导、血管平滑肌收缩、代谢途径等通路。KEGG通路分析发现，DEGs主要富集于环磷酸鸟苷（cGMP）-蛋白激酶G(PKG)信号通路、肥厚型心肌病和扩张型心肌病等信号通路。通过PPI网络，筛选出6个关键基因，分别是Gprc6a、C3、Anxa1、Oxt、Gpr4和Avpr1b，并发现有528个转录因子对这6个关键基因进行转录调节。qPCR结果显示，心力衰竭情况下Anxa1和Gpr4的mRNA表达差异有统计学意义，进一步验证了以上筛选结果。结论 通过生物信息学分析方法发现了6个与心力衰竭相关的关键基因，有助于更好地了解心力衰竭的发生机制和探索新的治疗靶点。

关键词(KeyWords)： 心力衰竭;差异表达基因;生物信息学

Abstract:

Keywords:

基金项目(Foundation): 国家自然科学基金（82170523）;; 山西省基础研究计划青年科学研究项目（202103021223238）;; 山西省自然科学研究面上项目（202303021211110）~~

作者(Author): 陈淼然,郭可欣,贺忠梅,宁俊娅,封启龙,高丽娟,曹济民

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