ArticleMolecular biotechnology2026
GINS4 Promotes Neonatal Bronchopulmonary Dysplasia via Driving Phosphorylation and Acetylation of p65 NF-κB.
Article in Molecular biotechnology, 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
As a recognized common and severe chronic disease predominantly affecting preterm infants, bronchopulmonary dysplasia (BPD) necessitates meticulous clinical management. Emerging evidence has thoroughly elucidated the role of complex subunit 4 (GINS4) in lung carcinogenesis. Nevertheless, the specific molecular mechanisms underlying GINS4' potential involvement in BPD pathogenesis remain underexplored and require systematic investigation. In this study, we proved that GINS4 expression was significantly upregulated in hyperoxia-induced lung injury. Additionally, in a hyperoxia-induced BPD neonatal rat model, GINS4 was found to upregulate the expression of inflammatory cytokines, including interleukin-6 (IL-6), interleukin-1β (IL-1β), interleukin-18 (IL-18), interferon-γ (IFN-γ), and tumor necrosis factor-α (TNF-ɑ), concomitantly increasing myeloperoxidase (MPO) activity. Histopathological analyses via Giemsa staining and hematoxylin-eosin (H&E) staining further revealed that GINS4 promoted alveolarization in this experimental context. Analysis of Aquaporin 5 (AQP5) and surfactant-associated protein C (SPC) indicated GINS4 exerted differential effects on alveolar development. Notably, GINS4 was found to directly interact with p65, thereby promoting phosphorylation and acetylation of the p65 NF-κB. Finally, in a preterm rat model, we demonstrate that GINS4 induced BPD-like pathological alterations in lung tissues, characterized by alveolar septal simplification and thickening. Collectively, this study identifies GINS4 as a potential novel therapeutic target for prevention and treatment of BPD.
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