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pmid:40838416
The NEAT1/miR-124-3p/CCL2 axis in chronic kidney disease progression: integrated bioinformatics analysis and experimental validation.
Guanting Chen · Linqi Zhang · Yaoxian Wang · Jianfeng Wang · Kang Yang · Xixi Wang · Xu Chen
Epigenomics · 2025 doi:10.1080/17501911.2025.2548762
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Experiment
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Analysis
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Complete file
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This study aimed to identify novel diagnostic biomarkers and therapeutictargets.\nRESEARCH DESIGN AND METHODS: Weanalyzed the GEO dataset GSE137570 to identify differentially expressed genes(DEGs). Protein-protein interaction (PPI) networks were constructed to screen HubGenes. A competing endogenous RNA (ceRNA) network was predicted. Validationincluded single-cell sequencing, in vitro epithelial-mesenchymal transition(EMT) models using Transforming growth factor-β 1 (TGF-β1)-treated TCMK1 cells,clinical samples (64 CKD patients, 20 healthy controls), and dual-luciferasereporter assays (DLRA).\nRESULTS: FiveHub Genes (EGF, VCAN, CXCL1, MMP7, CCL2) were identified, with CCL2 being themost central. Enrichment analyses linked them to immune/inflammatory responses.DLRA confirmed specific targeting between miR-124-3p and both NEAT1 and CCL2,supporting the NEAT1/miR-124-3p/CCL2 axis. Clinically, serum CCL2 increasedwhile miR-124-3p and NEAT1 decreased with CKD progression; all three showedgood diagnostic accuracy for staging.\nCONCLUSIONS: EGF,VCAN, CXCL1, MMP7, and particularly CCL2 are potential CKDbiomarkers/therapeutic targets. The NEAT1/miR-124-3p/CCL2 axis is a keyregulatory pathway in CKD. 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