ArticlePediatric research2026
Investigating mitophagy mechanisms in bronchopulmonary dysplasia through bioinformatics.
Article in Pediatric research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
1 citing paper in PubMed.
- Reconceptualizing chorioamnionitis as an immune-mediated inflammatory disorder at the maternal-fetal interface.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundBronchopulmonary dysplasia (BPD) is a prevalent respiratory disease in premature infants and is accompanied by impaired lung function, increased infection risk, and other long-term complications. This study aimed to elucidate the molecular mechanisms of BPD, especially mitophagy.
methodsBioinformatics analyses were performed to identify differentially expressed genes (DEGs) in BPD. Weighted gene co-expression network analysis (WGCNA) was used to explore gene modules associated with mitophagy, functional enrichment analyses to identify key biological processes, and immune infiltration to assess immune cell differences.
resultsAmong the 720 DEGs identified, 419 were upregulated and 301 were downregulated: these may serve as potential BPD biomarkers. WGCNA revealed that the turquoise module was strongly related to mitophagy (r = -0.6061, p < 0.05), indicating its significance in BPD pathogenesis. Enrichment analyses highlighted leukocyte migration and neutrophil extracellular trap formation, suggesting immune-mediated inflammatory response. Eight hub genes (S100P, CDC42EP3, CEACAM3, CKLF, RGL4, DOK3, B4GALT5, and MCEMP1) were identified as potential therapeutic targets. Immune infiltration analysis revealed significant differences in neutrophils and activated CD8+T cells, underscoring the immune system's role in BPD.
conclusionKey molecular players and pathways involved in BPD were elucidated, providing insights for future targeted therapies addressing immunity and mitophagy in BPD. IMPACT: This study identifies CEACAM3 and CDC42EP3 as key genes involved in mitophagy and immune dysregulation in bronchopulmonary dysplasia (BPD). It provides novel insights into the TNF-α/NF-κB signaling pathway and its role in the pathogenesis of BPD. This study advances biomarker discovery by associating CEACAM3 with neutrophil infiltration and CDC42EP3 with CD8+ T cell activity. The selected machine learning and bioinformatics approaches enhance the diagnostic accuracy and therapeutic targeting of BPD. These findings lay the foundation for future translational research in guiding personalized interventions for high-risk neonates.
Indexed as
Identifiers
40783597What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.