Abstract
Lupus nephritis (LN) is a common and severe organ manifestation of systemic lupus erythematosus (SLE) and is a major cause of SLE related deaths. Early diagnosis is essential to improve the prognosis of patients with LN. To screen the potential biomarkers associated with LN, we downloaded the gene expression profile of GSE99967 from the Gene Expression Omnibus (GEO) database. Weighted gene co-expression network analysis (WGCNA) was utilized to construct a gene co-expression network and identify gene modules associated with LN. Gene Ontology (GO) analysis was also applied to explore the biological function of genes and identify the key module. Differentially expressed genes (DEGs) were identified and Maximal Clique Centrality (MCC) values were calculated to screen hub genes. Furthermore, we selected promising biomarkers for real-time PCR (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA) validation in independent cohorts. Our results indicated that five hub genes, including IFI44, IFIT3, HERC5, RSAD2, and DDX60 play vital roles in the pathogenesis of LN. Importantly, IFI44 may considered as a key biomarker in LN for its diagnostic capabilities, which is also a promising therapeutic target in the future.
Highlights
Systemic lupus erythematosus (SLE) is an autoimmune disease involving an inappropriate immune response to endogenous nuclear particles, which affects multiple organs and systems [1]
The results showed that they were both elevated in class III(±V), class IV(±V), and class V compared with healthy controls (HCs) (Supplementary Figure 7), meaning that both interferon induced protein 44 (IFI44) and IFIT3 can indicate the prognosis of Lupus nephritis (LN)
Lupus nephritis is a major cause of morbidity and mortality in systemic lupus erythematosus (SLE), and many patients end in chronic kidney disease (CKD) or end-stage renal disease (ESRD) due to limited drug treatment [17, 18]
Summary
Systemic lupus erythematosus (SLE) is an autoimmune disease involving an inappropriate immune response to endogenous nuclear particles, which affects multiple organs and systems [1]. Lupus nephritis (LN) is an immune complex glomerulonephritis that develops as one of the most common and severe target-organ manifestations of SLE [2]. 10–30% of LN patients progress to end-stage renal disease (ESRD) within 15 years after diagnosis, which is the major cause of mortality in SLE [3]. It is imperative to further study the pathogenesis of LN to contribute to the diagnosis and treatment of LN and improve the prognosis of patients with LN. Recent studies have shown that LN susceptibility genes, which break immune tolerance are involved in the pathogenesis of LN
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