ArticleEuropean journal of medical research2025
Inhibition of complement system-related gene ITGB2 attenuates epithelial-mesenchymal transition and inflammation in diabetic nephropathy.
Article in European journal of medical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- ITGB2 promotes HIF-1α/GLUT1 mediated glucose metabolic reprogramming in renal tubular epithelial cells to aggravate the progression of diabetic kidney disease.Cytotechnology · 2026Article
- Comprehensive Mendelian randomization analysis of inflammatory networks in diabetic nephropathy and pituitary adenoma: unveiling complex causal relationships.Discover oncology · 2025Article
- C3AR1 may aggravate diabetic nephropathy by mediating oxidative stress via ITGB2 regulation in renal tubular epithelial cells.PloS one · 2025Article
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4 authors.
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Abstract
purposeEmerging evidences have indicated a role of the complement system in the pathogenesis of diabetic nephropathy (DN). Thus, this study was conducted to explore the complement system-related key biomarkers for patients with DN.
methodsDN microarray datasets were downloaded from the GEO database, followed by differentially expressed genes (DEGs) screening. Complement system-related genes (CSRGs) were searched from various databases. Weighted Gene Co-expression Network Analysis (WGCNA) was employed to screen the DN-related genes, then the differential CSRGs (DCSRGs) were identified, followed by protein-protein interaction (PPI) network construction. In addition, key biomarkers were acquired by two machine learning algorithms, then immune infiltration analysis, Gene Set Enrichment Analysis (GSEA), and potential drugs screening were conducted. Quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) and western blotting were utilized to detect the ITGB2 expression. Then the cell viability, inflammatory factors, and the expression of epithelial-mesenchymal transition (EMT) and fibrosis markers were determined by using Cell Counting Kit-8 (CCK-8) assay, enzyme linked immunosorbent assay (ELISA), western blotting assays, respectively.
resultsIn total, 1012 DEGs and 974 DN-related genes were screened, and intersection analysis of the three (DN-related genes, DEGs and CSRGs) yielded 13 intersection genes, which were considered as the DCSRGs. Subsequently, 2 key biomarkers were identified by machine learning, namely VWF and ITGB2. The VWF and ITGB2 were both enriched in the pathways of chemokine signaling pathway, CAMs, focal adhesion and natural killer cell-mediated cytotoxicity, and significantly correlated with the activated mast cells, resting NK cells, and macrophages. Also, VWF and ITGB2 were significantly related to the clinical features, including age, serum creatinine level, and GFR (MDRD). Besides, mRNA and protein expression levels of ITGB2 in HG-treated HK-2 cells were remarkably elevated. Moreover, the viability of HK-2 cells, expression of TNF-α, IL-6, IL-12, α-SMA, E-cadherin and vimentin in HK-2 cells changed by HG administration were reversed by ITGB2-silence.
conclusionComplement system-related gene ITGB2 was overexpressed in DN, and inhibition of ITGB2 attenuated EMT and inflammation in DN.
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