ArticleBiochemical genetics2026
The LINC00920/miR-6834-3p/CPN1 Axis Modulates Immune Dysregulation in Sepsis-Associated Acute Kidney Injury and Serves as a Diagnostic Biomarker.
Article in Biochemical genetics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Sepsis-associated acute kidney injury (SA-AKI) is a serious complication with high mortality and lacks effective diagnostic and treatment strategies. This study aims to investigate the role of the LINC00920/miR-6834-3p/CPN1 axis in SA-AKI and evaluate its diagnostic value. Clinical serum samples and in vitro cell models were used to explore the role of the LINC00920/miR-6834-3p/CPN1 axis in SA-AKI. Serum expression of LINC00920, miR-6834-3p and CPN1 was detected to analyze their expression patterns in SA-AKI, and their diagnostic value was evaluated to verify potential biomarker utility. Dual-luciferase reporter assay, mutant construct and rescue experiments were performed to confirm the regulatory relationship of the LINC00920/miR-6834-3p/CPN1 axis. Functional experiments were conducted to detect cell injury, macrophage polarization and NET formation, so as to clarify the biological function of the axis in SA-AKI progression. Clinical analysis showed LINC00920 and CPN1 were downregulated, miR-6834-3p upregulated in SA-AKI. LINC00920 was negatively correlated with SA-AKI severity, suggesting its association with disease progression. The LINC00920/miR-6834-3p/CPN1 panel had high diagnostic value for SA-AKI and severity (AUC = 0.913, 0.912). In vitro experiments confirmed LINC00920 acts as a ceRNA to sponge miR-6834-3p and upregulate CPN1, exerting a protective role in SA-AKI by alleviating cell injury, M1 polarization and NET formation. The LINC00920/miR-6834-3p/CPN1 axis regulates SA-AKI progression, correlates with disease severity, and is a promising diagnostic biomarker.
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