Abstract

Lupus Nephritis (LN) is one of the commonest complications of systemic lupus erythematosus which is characterized by autoimmune and tissue destruction. Elucidating the process in detail would be of great significance for clinical practice, however, the molecular mechanism underlying LN is not clear. In the study, GSE112943 and GSE81622 were retrieved from Gene Expression Omnibus database (GEO), and the differentially expressed genes (DEGs) were identified by GEO2R. Among these DEGs, 42 genes were up-regulated, and 7 genes were down-regulated. The functions and signaling pathways of these DEGs were analyzed systematically, and protein-protein interaction (PPI) networks of these DEGs were established through the search tool for the retrieval of interacting genes (STRING) database. 10 hub genes (IFI44, RSAD2, IFI44L, IFI27, MX1, IFIT3, IFIT1, IFI6, OAS3 and IFIT2) were screened out by the plug-in CytoHubba in Cytoscape. Expression level, diagnosis value as well as correlation with glomerular filtration rate (GFR) expression of these hub genes for LN patients were investigated in GEO datasets and Nephroseq v5 online platform. The results showed that eight of these hub genes were found highly expressed in LN tissues and significantly related to the diagnosis (AUC>0.7; p<0.05). In addition, these hub genes were negatively related to the GFR level of LN patients. In conclusion, the hub genes and pathways that were related to the development of LN were screened out, which could provide a new insight for the future molecularly targeted therapy and diagnostic evaluation. Key words: Lupus Nephritis (LN), Bioinformatics, Differentially Expressed Genes (DEGs), Hub Genes, diagnosis.

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.