慢性牙周炎与帕金森病之间的潜在关联。

Rongxia Yang, Yingrui Zong, Chen Zhang
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引用次数: 0

摘要

研究目的本研究旨在调查慢性牙周炎(CP)和帕金森病(PD)之间可能的枢纽基因、相关通路和转录因子:方法:从基因表达总库(GEO)中下载 CP(GSE16134、GSE23586 和 GSE10334)和 PD(GSE20141 和 GSE49036)的基因表达谱,进行差异表达分析和功能聚类分析。构建了蛋白质-蛋白质相互作用(PPI)网络,并通过四种拓扑分析算法和模块化分割筛选了枢纽基因。进行了功能聚类分析。通过CP和PD的外部数据集验证了中心基因,并通过孟德尔随机化(MR)进一步评估了因果关系:合并数据后,CP 数据集中筛选出 1 211 个差异表达基因(DEG),其中 551 个上调,660 个下调。PD 数据集共筛选出 2 407 个 DEGs,其中 1 438 个上调,969 个下调。PPI网络包括145个节点和126条边。最终筛选出四个枢纽基因(FCGR3B、PRF1、IL18 和 CD33)和三个转录因子(HSF1、HSF2 和 HSF4)。相关途径主要是自然杀伤(NK)细胞介导的毒性效应。磁共振结果表明,CP 与罹患帕金森病的风险之间可能存在正向因果关系:这项研究表明,CP 和 PD 之间可能存在共同的病理生理学和因果关系,并为未来的机理研究提供了新的概念和治疗靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Potential correlation between chronic periodontitis and Parkinson's disease.

Objectives: This study aims to investigate possible hub genes, associated pathways, and transcription factors between chronic periodontitis (CP) and Parkinson's disease (PD).

Methods: Gene expression profiles of CP (GSE16134, GSE23586, and GSE10334) and PD (GSE20141 and GSE49036) were downloaded from the gene expression omnibus (GEO) database for differential expression analysis and functional clustering analysis. The protein-protein interaction (PPI) network was constructed, and hub genes were screened by four topological analysis algorithms and modular segmentation. Functional clustering analysis was performed. The hub genes were validated by external datasets of CP and PD, and causal relation was further assessed by Mendelian randomization (MR).

Results: After merging the data, 1 211 differentially expressed genes (DEGs) were screened in the CP datasets; of which, 551 were upregulated and 660 were downregulated. A total of 2 407 DEGs were screened in the PD dataset, of which, 1 438 were upregulated and 969 were downregulated. The PPI network included 145 nodes and 126 edges. Four hub genes (FCGR3B, PRF1, IL18, and CD33) and three transcription factors (HSF1, HSF2, and HSF4) were finally screened. The relevant pathway was predominantly natural killer (NK) cell-mediated toxic effects. The MR results suggest a possible positive causal relationship between CP and the risk of developing PD.

Conclusions: This study indicated the probably shared pathophysiology and possible causal relationship between CP and PD and may offer novel concepts and therapeutic targets for future mechanistic investigations.

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