ArticleBMC immunology2026
miR-379-5p serves as a biomarker and regulates sepsis-associated acute kidney injury via targeting EDN1.
Article in BMC immunology, 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
backgroundSepsis-associated acute kidney injury (SA-AKI) is a serious complication for sepsis patients, and microRNA (miRNA) is involved in its occurrence and development. This study investigated the clinical value of miR-379-5p and its potential mechanism on LPS-induced human proximal tubular epithelial cell lines (HK-2).
methodsSerum miR-379-5p levels were measured in 85 sepsis patients and 74 SA-AKI patients. The clinical significance of miR-379-5p was explored from the perspectives of SA-AKI diagnosis, kidney injury correlation, and 28-day survival assessment. The LPS-induced HK-2 cell model was constructed, and the regulatory effect of miR-379-5p on LPS-induced HK-2 cell viability and inflammatory response was analyzed. The regulatory mechanism was explored, focusing on the involvement of EDN1.
resultsLow expression of serum miR-379-5p could distinguish SA-AKI from sepsis patients and was negatively correlated with serum creatinine (Scr), blood urea nitrogen (BUN), cystatin-C (Cys-C), kidney injury molecule-1 (KIM-1), C-reactive protein (CRP), procalcitonin (PCT), and white blood cell (WBC). Low expression of miR-379-5p was correlated with the 28-day survival rate. LPS could inhibit the expression of miR-379-5p in HK-2 cells, inhibit cell viability, and promote the concentration of inflammatory factors TNF-α, IL-1β, and IL-6. Overexpression of miR-379-5p reversed the effect of LPS on HK-2 cells. EDN1 was a direct target gene of miR-379-5p. Overexpression of EDN1 counteracted the protective effect of miR-379-5p overexpression on HK-2 cells.
conclusionsDownregulated serum miR-379-5p had the potential value in diagnosing SA-AKI and forecasting 28-day patient survival. Overexpression of miR-379-5p protected HK-2 cells from LPS-induced injury by targeting and inhibiting EDN1.
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