ArticleBMC pediatrics2026
MIR210HG promotes the progression of pediatric pneumonia by inducing apoptosis and inflammation through downregulating miR-195-5p and upregulating FGF2.
Article in BMC pediatrics, 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
objectiveIf 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.
methodsA 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.
resultsMIR210HG 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.
conclusionMIR210HG 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.
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