ArticleFrontiers in physiology2026
Hyperoxia promotes bronchopulmonary dysplasia via Noggin-mediated BMP4 antagonism and cellular senescence.
Article in Frontiers in physiology, 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
Bronchopulmonary dysplasia (BPD) represents the most prevalent chronic pulmonary complication in preterm infants, with incompletely understood pathophysiological mechanisms. Hyperoxia exposure constitutes a major risk factor for BPD development, inducing cellular senescence that impairs alveolar maturation. While senescence is predominantly mediated by the p53/p21 signaling pathway, upstream regulatory mechanisms remain inadequately defined. This study aimed to identify critical genes through bioinformatics and elucidate the molecular mechanisms by which the Noggin-BMP4 signaling axis mediates cellular senescence in BPD pathogenesis. Integrating BPD transcriptomic datasets with aging-related databases via WGCNA, Noggin was identified as a hub gene linking BPD and cellular senescence (AUC = 0.80). In HPMECs exposed to 85% hyperoxia, Noggin expression increased approximately 2.5-fold (mRNA) and 2.0-fold (protein), while BMP4 decreased to 50% of controls, accompanied by elevated p53 and p21 expression and positive SA-β-gal staining. Noggin silencing restored BMP4 expression and significantly attenuated hyperoxia-induced p53/p21 upregulation, suggesting that Noggin promotes senescence by suppressing BMP4. In a neonatal rat hyperoxia-induced BPD model, alveolar simplification was observed alongside a threefold increase in Noggin mRNA, a reduction of BMP4 to 30% of controls, and elevated p53/p21 at day 14, corroborating the
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