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已发表论文
糖尿病肾病中糖基化相关基因及预后特征
Authors Li X, Sun T, Li X, Li H , Zheng X, Zhang Y, Yu W, Liu Y, Shang J, Xiao J, Zhao Z
Received 7 June 2025
Accepted for publication 27 October 2025
Published 22 November 2025 Volume 2025:18 Pages 7075—7094
DOI https://doi.org/10.2147/IJGM.S545376
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Professor David E. Stec
Xiaohui Li,1 Tao Sun,2 Xiaoqian Li,1 Huangmin Li,1 Xuejun Zheng,1 Yiding Zhang,1 Wei Yu,1 Yifei Liu,3 Jin Shang,1 Jing Xiao,1 Zhanzheng Zhao1
1Department of Nephrology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, 450052, People’s Republic of China; 2Henan Medical College, Zhengzhou, Henan, 451191, People’s Republic of China; 3Department of Nephrology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, 410011, People’s Republic of China
Correspondence: Jing Xiao, Email xiaojing5123@139.com Zhanzheng Zhao, Email zhanzhengzhao@zzu.edu.cn
Background: Diabetic nephropathy (DN) is the leading cause of end-stage renal disease worldwide, whose pathogenesis involves immune dysregulation and inflammatory response. Glycosylation plays key roles in numerous biological processes. This study aims to interrogate the role of glycosylation-related genes in tubulointerstitial immunoinflammatory injury in DN.
Methods: We utilized two tubulointerstitial transcriptome datasets from DN patients and normal individuals. Glycosylation-related hub genes were identified by integrating differential expression analysis, glycosylation-related gene sets, and machine learning. Immune cell infiltration was assessed using single-sample GSEA (ssGSEA), and functional enrichment analysis was performed via GO and KEGG. The expression levels of hub genes were validated in STZ-induced diabetic mouse model (n=5/group) followed by the evaluation of diagnostic efficiency and clinical significance.
Results: Six glycosylation-related hub genes (HEXB, B4GALT5, GALNT7, GCNT3, CGA, and VCAN) were identified, all closely associated with immune cell infiltration in DN. Enrichment analysis indicated their involvement in immune and inflammatory processes. CGA was significantly downregulated, while the other genes were upregulated in DN, which was experimentally validated in diabetic mice. ROC curve analysis revealed high diagnostic accuracy for all genes: HEXB (AUC = 0.892), B4GALT5 (AUC = 0.909), GALNT7 (AUC = 0.931), GCNT3 (AUC = 0.929), CGA (AUC = 0.898), and VCAN (AUC = 0.967). Elevated VCAN, GCNT3, and GALNT7 exhibited a positive association with renal function decline or proteinuria, providing valuable prognostic insights.
Conclusion: This study highlights the significant role of glycosylation-related genes in DN pathogenesis, likely mediated through immune and inflammatory mechanisms. VCAN, GCNT3, and GALNT7 show particular promise as novel biomarkers for clinical diagnosis and immunotherapeutic targets, supporting their future clinical translation for DN management.
Keywords: diabetic nephropathy, glycosylation, bioinformatics analysis, immune infiltration
1Department of Nephrology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, 450052, People’s Republic of China; 2Henan Medical College, Zhengzhou, Henan, 451191, People’s Republic of China; 3Department of Nephrology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, 410011, People’s Republic of China
Correspondence: Jing Xiao, Email xiaojing5123@139.com Zhanzheng Zhao, Email zhanzhengzhao@zzu.edu.cn
Background: Diabetic nephropathy (DN) is the leading cause of end-stage renal disease worldwide, whose pathogenesis involves immune dysregulation and inflammatory response. Glycosylation plays key roles in numerous biological processes. This study aims to interrogate the role of glycosylation-related genes in tubulointerstitial immunoinflammatory injury in DN.
Methods: We utilized two tubulointerstitial transcriptome datasets from DN patients and normal individuals. Glycosylation-related hub genes were identified by integrating differential expression analysis, glycosylation-related gene sets, and machine learning. Immune cell infiltration was assessed using single-sample GSEA (ssGSEA), and functional enrichment analysis was performed via GO and KEGG. The expression levels of hub genes were validated in STZ-induced diabetic mouse model (n=5/group) followed by the evaluation of diagnostic efficiency and clinical significance.
Results: Six glycosylation-related hub genes (HEXB, B4GALT5, GALNT7, GCNT3, CGA, and VCAN) were identified, all closely associated with immune cell infiltration in DN. Enrichment analysis indicated their involvement in immune and inflammatory processes. CGA was significantly downregulated, while the other genes were upregulated in DN, which was experimentally validated in diabetic mice. ROC curve analysis revealed high diagnostic accuracy for all genes: HEXB (AUC = 0.892), B4GALT5 (AUC = 0.909), GALNT7 (AUC = 0.931), GCNT3 (AUC = 0.929), CGA (AUC = 0.898), and VCAN (AUC = 0.967). Elevated VCAN, GCNT3, and GALNT7 exhibited a positive association with renal function decline or proteinuria, providing valuable prognostic insights.
Conclusion: This study highlights the significant role of glycosylation-related genes in DN pathogenesis, likely mediated through immune and inflammatory mechanisms. VCAN, GCNT3, and GALNT7 show particular promise as novel biomarkers for clinical diagnosis and immunotherapeutic targets, supporting their future clinical translation for DN management.
Keywords: diabetic nephropathy, glycosylation, bioinformatics analysis, immune infiltration