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<p>Diabetic nephropathy (DN) is a prevalent and serious complication of diabetes, characterized by chronic inflammation and progressive kidney damage. This study aimed to investigate the role of immune checkpoint-related genes (ICGs) in the pathogenesis of DN. We integrated and analyzed gene expression data of DN patients from multiple GEO databases and identified 33 differentially expressed ICGs. Functional enrichment analysis revealed that these genes are involved in immune response and inflammation-related pathways. Immune cell infiltration analysis indicated a significant increase in immune cell abundance in the kidneys of DN patients. CSF1R was consistently identified as a key gene using various methods, including LASSO regression, machine learning algorithms (GLM, RF, SVM, XGB), and WGCNA analysis focusing on both disease-related and cluster-related modules. The identification of CSF1R was further validated in an external dataset and single-cell RNA sequencing data. CSF1R was upregulated in DN patients and played a crucial role in regulating immune responses and inflammation. In vitro and in vivo experiments confirmed the involvement of CSF1R in renal fibrosis, indicating its potential as a therapeutic target for DN. This study provides valuable insights into the role of ICGs and CSF1R in the pathogenesis of DN and suggests their potential as targets for diagnosis and treatment.</p>

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Potential implications of targeting CSF1R in diabetic nephropathy associated fibrosis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年8月5日

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  • Dongshan Chen,
  • Zihao Gao,
  • Haochen Cui,
  • Chenfei Wang,
  • Cong Zhang,
  • Dong Wu,
  • Yuanwei Zang

摘要

Diabetic nephropathy (DN) is a prevalent and serious complication of diabetes, characterized by chronic inflammation and progressive kidney damage. This study aimed to investigate the role of immune checkpoint-related genes (ICGs) in the pathogenesis of DN. We integrated and analyzed gene expression data of DN patients from multiple GEO databases and identified 33 differentially expressed ICGs. Functional enrichment analysis revealed that these genes are involved in immune response and inflammation-related pathways. Immune cell infiltration analysis indicated a significant increase in immune cell abundance in the kidneys of DN patients. CSF1R was consistently identified as a key gene using various methods, including LASSO regression, machine learning algorithms (GLM, RF, SVM, XGB), and WGCNA analysis focusing on both disease-related and cluster-related modules. The identification of CSF1R was further validated in an external dataset and single-cell RNA sequencing data. CSF1R was upregulated in DN patients and played a crucial role in regulating immune responses and inflammation. In vitro and in vivo experiments confirmed the involvement of CSF1R in renal fibrosis, indicating its potential as a therapeutic target for DN. This study provides valuable insights into the role of ICGs and CSF1R in the pathogenesis of DN and suggests their potential as targets for diagnosis and treatment.