miR-4772-3p serves as a potential diagnostic and prognostic biomarker in septic acute kidney injury by targeting CISD2

This study aims to explore the clinical value and function of miR-4772-3p in septic acute kidney injury (AKI). A total of 99 septic patients without AKI and 93 with AKI were enrolled. RT-qPCR measured miR-4772-3p expression. Diagnostic and predictive value was assessed using the ROC curve and logistic regression, and prognostic utility was evaluated by Kaplan-Meier and Cox regression. An lipopolysaccharide (LPS)-induced human kidney‑2 cell line (HK-2) cell model was established to assess viability by CCK-8, apoptosis by flow cytometry, inflammatory cytokines (tumor necrosis factor‑α (TNF‑α), interleukin‑6 (IL‑6), interleukin‑1β (IL‑1β)) by ELISA, and oxidative stress (superoxide dismutase (SOD) and malondialdehyde (MDA)). Bioinformatics and dual-luciferase assay identified the targets of miR-4772-3p. miR‑4772‑3p was upregulated in septic AKI, and its level positively correlated with cystatin C (Cys‑C), serum creatinine (Scr), Sequential Organ Failure Assessment (SOFA) score, Acute Physiology and Chronic Health Evaluation II (APACHE II) score, blood urea nitrogen (BUN), and estimated glomerular filtration rate (eGFR). miR‑4772‑3p showed high diagnostic value and was an independent risk factor for AKI occurrence. Moreover, higher miR‑4772‑3p expression was linked to elevated mortality and served as an independent prognostic risk factor. In the LPS‑induced HK‑2 model, decreased cell viability, increased apoptosis, elevated pro‑inflammatory cytokines (TNF-α, IL-6, IL-1β), reduced SOD activity, and increased MDA content were observed. Inhibition of miR‑4772‑3p reversed these injury phenotypes. Mechanistically, CDGSH iron sulfur domain 2 (CISD2) was verified as a direct target gene of miR‑4772‑3p; knockdown of CISD2 could reverse the effects of miR-4772-3p inhibition in pathological regulation. miR‑4772‑3p may serve as a potential diagnostic and prognostic biomarker for septic AKI. Its upregulation may promote sepsis-induced HK-2 cell injury by regulating CISD2, thereby facilitating AKI progression.