ArticleCentral-European journal of immunology2025
lncRNA FENDRR targets miR-3614-5p to promote sepsis-induced acute kidney injury
Article in Central-European journal of immunology, 2025. 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
Introduction: Acute kidney injury (AKI) raises mortality rates in septic patients. This study investigated the relationship between lncRNA FENDRR and miR-3614-5p, aiming to examine FENDRR's clinical significance in sepsis-induced AKI and identify new diagnostic biomarkers. Material and methods: Eighty-five patients with sepsis-induced AKI and 90 patients with sepsis were included. ROC curve and multivariate logistic analysis were performed to assess the diagnostic value of FENDRR and risk factors, respectively. The binding between FENDRR and miR-3614-5p was detected by the dual-luciferase reporter assay. An inflammatory cell model was constructed using lipopolysaccharide (LPS) to verify the effects of FENDRR on cell function and inflammation. Results: FENDRR was down-regulated and miR-3614-5p was up-regulated in AKI patients, with a negative correlation and target-binding relationship. FENDRR has potential diagnostic value in differentiating between patients with sepsis-induced AKI and those with sepsis. FENDRR is a risk factor for sepsis-induced AKI. Procalcitonin (PCT), blood urea nitrogen (BUN), serum creatinine (SCr), Acute Physiology and Chronic Health Evaluation II (APACHE II), Sequential Organ Failure Assessment (SOFA), lactate, and length of hospital stay were positively correlated with FENDRR in AKI patients. Silencing of FENDRR alleviated the LPS-induced increase in MDA content, reactive oxygen species (ROS), levels of inflammatory factors, and renal injury markers in HK-2 cells while mitigating the LPS-induced increase in apoptosis rate and decrease in cellular activity. Conclusions: FENDRR serves as a biomarker for sepsis-induced AKI. FENDRR inhibits miR-3614-5p to regulate cellular inflammation and oxidative damage and plays a crucial role in the pathogenesis of sepsis-induced AKI.
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