脓毒症心肌病中嗜中性粒细胞相关枢纽基因的生物信息学分析和 ceRNA 网络构建

IF 3.9 3区 医学 Q2 CELL BIOLOGY
Aging-Us Pub Date : 2024-08-30 DOI:10.18632/aging.206092
Qingfei Cao, Jing Li, Meixue Chen
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引用次数: 0

摘要

脓毒性心肌病(SCM)是一种重要的脓毒症并发症,其特点是在早期脓毒性休克期间出现可逆性心脏抑制。中性粒细胞是先天性免疫不可或缺的组成部分,一旦出现异常,就会介导器官损伤,但它们在脓毒症诱发的心肌损伤中的具体作用仍然难以捉摸。我们的研究重点是阐明中性粒细胞相关基因(NRGs)在SCM中的作用,寻找早期诊断和治疗的生物标志物。我们从数据集 GSE79962 和 GSE44363 中确定了共有的差异表达基因(DEGs),并使用 Cytoscape 软件中的 cytoHubba 插件精确定位了中枢 DEGs。中性粒细胞相关枢纽基因(NRHG)MRC1 是通过枢纽 DEG 与 WGCNA 中的 NRG 相互交叉而确定的。我们利用自己的数据和外部数据集验证了 MRC1 在单核细胞增多症中的异常表达。此外,我们还构建并验证了中性粒细胞相关的 ceRNA 网络(AC145207.5/ miR-23a-3p/MRC1)。我们的研究结果揭示了 MRC1 是单核细胞增多症发病机制中潜在的 NRHG,为了解单核细胞增多症中中性粒细胞介导的机制提供了见解,并为单核细胞增多症的早期诊断和干预提供了一个新的分子靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Bioinformatics analysis of neutrophil-associated hub genes and ceRNA network construction in septic cardiomyopathy.

Septic cardiomyopathy (SCM) is a critical sepsis complication characterized by reversible cardiac depression during early septic shock. Neutrophils, integral to innate immunity, can mediate organ damage when abnormal, but their specific role in sepsis-induced myocardial damage remains elusive. Our study focuses on elucidating the role of Neutrophil-Related Genes (NRGs) in SCM, finding early diagnosis and treatment biomarkers. We identified shared differentially expressed genes (DEGs) from datasets GSE79962 and GSE44363 and pinpointed hub DEGs using the cytoHubba plugin in Cytoscape software. The Neutrophil-Related Hub Gene (NRHG) MRC1 was identified via intersecting hub DEGs with NRGs from WGCNA. We validated MRC1's abnormal expression in SCM using our data and external datasets. Furthermore, a neutrophil-related ceRNA network (AC145207.5/ miR-23a-3p/MRC1) was constructed and validated. Our findings reveal MRC1 as a potential NRHG in SCM pathogenesis, offering insights into neutrophil-mediated mechanisms in SCM and providing a novel molecular target for early diagnosis and intervention in SCM.

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来源期刊
Aging-Us
Aging-Us CELL BIOLOGY-
CiteScore
10.00
自引率
0.00%
发文量
595
审稿时长
6-12 weeks
期刊介绍: Information not localized
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