Silencing miR-483-5p may attenuate inflammatory responses in the in vitro LN cell model via targeting FOXO3

Dysregulated microRNAs (miRNAs) are intricately associated with the pathogenesis of lupus nephritis (LN). This research centers on miR-483-5p, whose role and molecular mechanism in LN remain largely unclear. The objective of this study is to explore the expression pattern, diagnostic value, and functional mechanism of miR-483-5p in LN, as well as its targeting regulatory relationship with Forkhead box O3 (FOXO3). Serum samples from LN patients and healthy controls were gathered to detect miR-483-5p and FOXO3 by RT-qPCR. LPS-induced Human renal glomerular mesangial cells (HRMCs) were used as the in vitro LN model. Cell proliferation was examined via the CCK-8 assay, and inflammatory cytokines were measured via ELISA. Dual-luciferase reporter and RIP assays validated the relationship between miR-483-5p and FOXO3. Rescue experiments were carried out to confirm the regulatory axis. The levels of miR-483-5p were elevated in the serum of patients with LN, demonstrating favorable diagnostic efficacy and a strong correlation with disease activity. In the LPS-induced LN cell model, miR-483-5p may regulate cell proliferation and the secretion of pro-inflammatory cytokines. FOXO3 may be identified as a target of miR-483-5p, and its content exhibited a negative correlation with miR-483-5p in LN. Silencing FOXO3 may reverse the inhibitory effects of the miR-483-5p inhibitor on LN cell dysfunction. miR-483-5p may regulate cell proliferation and inflammatory response in LN by targeting FOXO3.