ArticleRenal failure2025
Integration of transcriptome and Mendelian randomization analyses in exploring the extracellular vesicle-related biomarkers of diabetic kidney disease.
Article in Renal failure, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.
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Who cites it
2 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Exosomes in diabetic kidney disease: pathogenesis, biomarker discovery, and emerging therapeutics-a comprehensive systematic review.Renal failure · 2026Pooled it
- From pathogenic carriers to therapeutic hope: the dual role and translational prospects of exosomes in diabetic kidney disease.Frontiers in endocrinology · 2026Review
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDiabetic Kidney Disease (DKD) is a common complication in patients with diabetes, and its pathogenesis remains incompletely understood. Recent studies have suggested that extracellular vesicles (EVs) may play a significant role in the initiation and progression of DKD. This study aimed to identify biomarkers associated with EVs in DKD through bioinformatics and Mendelian randomization (MR) analysis.
methodsThis study utilized two DKD-related datasets, GSE96804 and GSE30528, alongside 121 exosome-related genes (ERGs) and 200 inflammation-related genes (IRGs). Differential analysis, co-expression network construction, and MR analysis were conducted to identify candidate genes. Machine learning techniques and expression validation were then employed to determine biomarkers. Finally, the potential mechanisms of action of these biomarkers were explored through Immunohistochemistry (IHC) staining, enrichment analysis, immune infiltration analysis, and regulatory network construction.
resultsA total of 22 candidate genes were identified as causally linked to DKD. CMAS and RGS10 were identified as biomarkers, with both showing reduced expression in DKD. IHC confirmed low RGS10 expression, providing new insights into DKD management. CMAS was involved primarily in mitochondria-related pathways, while RGS10 was enriched in the extracellular matrix and associated pathways. Significant differences were observed in neutrophils and M2 macrophages between DKD and normal groups, correlating strongly with the biomarkers.
conclusionThis study identified two EV-associated biomarkers, CMAS and RGS10, linked to DKD and elucidated their potential roles in disease progression. These results offer valuable insights for further exploration of DKD pathogenesis and the development of new therapeutic targets.
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