Abstract
OBJECTIVE: If not diagnosed and treated promptly, children pneumonia (CP) can lead to severe complications and even become life-threatening. MIR210HG is highly expressed in pneumonia patients. This study primarily investigates its diagnostic value and potential regulatory mechanisms in CP. METHODS: A total of 108 patients with CP were enrolled. PPI network analysis identified target genes of miR-195-5p. RT-qPCR detected levels of MIR210HG, miR-195-5p, and FGF2. Pearson correlation analysis examined the relationship between MIR210HG and miR-195-5p. ROC curve analysis evaluated the diagnostic value of MIR210HG. Cell proliferation, apoptosis, and the expression levels of apoptosis-related genes (Bax, Bcl-2, and caspase-3) and proinflammatory factors (TNF-α, IL-6, IL-1β) were assessed using CCK-8 assays, flow cytometry, and RT-qPCR, respectively. DLR experiments validated the binding relationship between miR-195-5p and MIR210HG and FGF2. RESULTS: MIR210HG levels were significantly elevated in both serum and BALF, with AUC values of 0.876 and 0.884, respectively. MIR210HG bound to miR-195-5p and exhibited a negative correlation with its expression. MIR210HG levels were elevated in CP models. Knockdown of MIR210HG promoted cell proliferation, inhibited apoptosis, and alleviated inflammatory responses by upregulating miR-195-5p levels. Furthermore, FGF2 is a target of miR-195-5p and is highly expressed in CP patients. CONCLUSION: MIR210HG shows promising diagnostic potential in CP patients. Our preliminary findings confirm that elevated MIR210HG may promote CP disease progression by downregulating FGF2 expression through miR-195-5p. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12887-026-06608-w.