ArticleHereditas2022
Identification of tubulointerstitial genes and ceRNA networks involved in diabetic nephropathy via integrated bioinformatics approaches.
Article in Hereditas, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- Mendelian randomization and single-cell transcriptomics prioritize CD7 and LAPTM5 in primary Sjögren's disease: an integrative multi-omics analysis.Clinical rheumatology · 2026Article
- Dynamic transcriptomic profiling of dorsal root ganglia reveals stage-specific mechanisms in diabetic neuropathic pain.Frontiers in molecular neuroscience · 2026Article
- Non-Coding RNA in Type 2 Diabetes Cardio-Renal Complications and SGLT2 Inhibitor Response.International journal of molecular sciences · 2025Review
- Research progress on non-coding RNA regulatory networks and targeted therapy in diabetic nephropathy.Frontiers in endocrinology · 2025Review
- Potential role of microRNA-503 in Icariin-mediated prevention of high glucose-induced endoplasmic reticulum stress.World journal of diabetes · 2023Article
- Integrative analyses of biomarkers and pathways for diabetic nephropathy.Frontiers in genetics · 2023Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDiabetic nephropathy (DN) is the major cause of end-stage renal disease worldwide. The mechanism of tubulointerstitial lesions in DN is not fully elucidated. This article aims to identify novel genes and clarify the molecular mechanisms for the progression of DN through integrated bioinformatics approaches.
methodWe downloaded microarray datasets from Gene Expression Omnibus (GEO) database and identified the differentially expressed genes (DEGs). Enrichment analyses, construction of Protein-protein interaction (PPI) network, and visualization of the co-expressed network between mRNAs and microRNAs (miRNAs) were performed. Additionally, we validated the expression of hub genes and analyzed the Receiver Operating Characteristic (ROC) curve in another GEO dataset. Clinical analysis and ceRNA networks were further analyzed.
resultsTotally 463 DEGs were identified, and enrichment analyses demonstrated that extracellular matrix structural constituents, regulation of immune effector process, positive regulation of cytokine production, phagosome, and complement and coagulation cascades were the major enriched pathways in DN. Three hub genes (CD53, CSF2RB, and LAPTM5) were obtained, and their expression levels were validated by GEO datasets. Pearson analysis showed that these genes were negatively correlated with the glomerular filtration rate (GFR). After literature searching, the ceRNA networks among circRNAs/IncRNAs, miRNAs, and mRNAs were constructed. The predicted RNA pathway of NEAT1/XIST-hsa-miR-155-5p/hsa-miR-486-5p-CSF2RB provides an important perspective and insights into the molecular mechanism of DN.
conclusionIn conclusion, we identified three genes, namely CD53, CSF2RB, and LAPTM5, as hub genes of tubulointerstitial lesions in DN. They may be closely related to the pathogenesis of DN and the predicted RNA regulatory pathway of NEAT1/XIST-hsa-miR-155-5p/hsa-miR-486-5p-CSF2RB presents a biomarker axis to the occurrence and development of DN.
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