背景:女性比男性更容易患上慢性疾病,进行性自身免疫性疾病被称为类风湿性关节炎(RA)。尽管基于性别的差异和自身免疫功能障碍之间可能存在复杂的相互作用。它们在RA中的功能在很大程度上是未知的,不过。这项研究的目的是查明控制男性和女性RA生物学变异的关键基因和代谢途径。
方法:首先,下载GSE39340和GSE55457的基因表达综合数据库基因表达信息(GEO)。使用R软件来找到性别之间的每个单独鉴定的差异表达基因(DEGs)。找到重叠的DEG。然后使用蛋白质-蛋白质相互作用(PPI)网络进一步检查重叠DEG之间的相互作用。京都基因和基因组百科全书和基因本体论工具,分别,用于进行富集分析。
结果:根据我们的发现,有1169个DEG在RA男性和女性之间重叠,包括845个上调基因和324个下调基因。十个枢纽基因,包括PIK3R1,RAC1,HRAS,PTPN11,UQCRB,NDUFV1,EGF,UBA1、UBE2G1和UBE2E1是在PPI网络中发现的。根据功能富集分析,这些基因主要富集在神经退行性疾病中,包括各种疾病途径,MAPK信号,胰岛素信号,和自噬。
结论:目前的数据表明MAPK通路和自噬可能是RA性别差异的重要因素。PTPN11,EGF,UBA1可能是与RA性别发展相关的重要基因,并有望成为该疾病的治疗靶标。我们的研究指出MAPK通路和自噬可能是RA性别差异的重要因素。•PTPN11,EGF,UBA1可能是与RA性别发展相关的重要基因,并有望成为该疾病的治疗靶标。•这些发现可能有助于开发男性和女性RA的新型诊断和治疗技术。
BACKGROUND: Women are more likely than men to develop the chronic, progressive autoimmune disease known as rheumatoid arthritis (RA). Although there may be a complex interplay between sex-based differences and autoimmune dysfunction. Their function in RA is largely unknown, though. The purpose of this study was to pinpoint the crucial genes and metabolic pathways that control biological variations in RA between men and women.
METHODS: First, the Gene Expression Omnibus database\'s gene expression information for GSE39340 and GSE55457 was downloaded (GEO). R software was used to find each of the individually identified differentially expressed genes (DEGs) between the sexes. DEGs that overlapped were found. The interactions between the overlapping DEGs were then further examined using a protein-protein interaction (PPI) network. The Kyoto Encyclopedia of Genes and Genomes and Gene Ontology tools, respectively, were used to perform enrichment analyses.
RESULTS: According to our findings, there were 1169 DEGs that overlapped between RA males and females, comprising 845 up-regulated genes and 324 down-regulated genes. Ten hub genes, including PIK3R1, RAC1, HRAS, PTPN11, UQCRB, NDUFV1, EGF, UBA1, UBE2G1, and UBE2E1, were discovered in the PPI network. According to a functional enrichment analysis, these genes were primarily enriched in neurodegenerative illnesses, including various disease pathways, MAPK signaling, insulin signaling, and autophagy.
CONCLUSIONS: The current data point to the possibility that the MAPK pathway and autophagy may be significant contributors to sex differences in RA. PTPN11, EGF, and UBA1 may be important genes linked to the gender development of RA and are anticipated to be therapeutic targets for the disease. Key Points • Our research point to the possibility that the MAPK pathway and autophagy may be significant contributors to sex differences in RA. • PTPN11, EGF, and UBA1 may be important genes linked to the gender development of RA and are anticipated to be therapeutic targets for the disease. • These findings may aid in the development of novel diagnostic and treatment techniques for RA in men and women.