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Identification of molecular subtypes of ischaemic stroke based on immune‐related genes and weighted co‐expression network analysis

Immune system has been reported to play a key role in the development of ischaemic stroke (IS). Nevertheless, its exact immune‐related mechanism has not yet been fully revealed. Gene expression data of IS and healthy control samples was downloaded from Gene Expression Omnibus database and differenti...

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Detalles Bibliográficos
Autores principales: Wei, Duncan, Chen, Xiaopu, Xu, Jing, He, Wenzhen
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10116020/
https://www.ncbi.nlm.nih.gov/pubmed/36802116
http://dx.doi.org/10.1049/syb2.12059
Descripción
Sumario:Immune system has been reported to play a key role in the development of ischaemic stroke (IS). Nevertheless, its exact immune‐related mechanism has not yet been fully revealed. Gene expression data of IS and healthy control samples was downloaded from Gene Expression Omnibus database and differentially expressed genes (DEGs) was obtained. Immune‐related genes (IRGs) data was downloaded from the ImmPort database. The molecular subtypes of IS were identified based on IRGs and weighted co‐expression network analysis (WGCNA). 827 DEGs and 1142 IRGs were obtained in IS. Based on 1142 IRGs, 128 IS samples were clustered into two molecular subtypes: clusterA and clusterB. Based on the WGCNA, the authors found that the blue module had the highest correlation with IS. In the blue module, 90 genes were screened as candidate genes. The top 55 genes were selected as the central nodes according to gene degree in protein–protein interactions network of all genes in blue module. Through taking overlap, nine real hub genes were obtained that might distinguish between clusterA subtype and clusterB subtype of IS. The real hub genes (IL7R, ITK, SOD1, CD3D, LEF1, FBL, MAF, DNMT1, and SLAMF1) may be associated with molecular subtypes and immune regulation of IS.