基因
败血症
计算生物学
医学
机制(生物学)
小桶
遗传学
生物
生物信息学
免疫学
基因本体论
基因表达
认识论
哲学
作者
Xuemeng Gao,Xiaofeng Zhou,Meng-wei Jia,Xiao-Zhuo Wang,Dan Liŭ
标识
DOI:10.1016/j.ypmed.2023.107540
摘要
When the body damages its own tissues in response to an infection, sepsis develops. Medical treatments are limited. It's important to understand the molecular mechanism behind sepsis pathogenesis and identify potential molecular treatment targets. We made two modules based on how genes work together by using WGCNA analysis. The light-green GSE131761 module and the blue GSE137342 module had the strongest links to sepsis. A gene ontology (GO) analysis showed that most of the genes in the lightgreen module were involved in the inflammatory response, specific granule, and immune receptor activity. Most of the genes in the blue module were significantly more likely to have the GO terms proteasomal protein catabolic process, ubiquitin ligase complex, and ubiquitin-like protein transferase activity. The KEGG analysis showed that the genes in module lightgreen were mostly involved in the TNF signaling pathway, while the genes in module blue were mostly involved in the Prion disease pathway. There were two hub genes that were found. In the end, ANKRD22 and VNN1 were singled out as crucial genes. This study used WGCNA to investigate sepsis-associated susceptibility modules and genes. Our study identified two modules and two key genes as essential components in sepsis etiology, which may improve our understanding of its molecular mechanisms.
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