Hanzhou Guan, Huaiqing Yin
Macrophage-related BPD research has shifted from early work on general inflammation and injury to more recent studies emphasizing gene regulation, signaling pathways, and pulmonary vascular complications. Key needs include stronger integration of human data with animal models, improved data standardization, and broader collaboration. Future studies should combine multi-omics with clinical outcomes to support immune-targeted and precision approaches for neonatal lung disease.
BACKGROUND: Bronchopulmonary dysplasia (BPD) remains a major complication of prematurity, and macrophages are increasingly recognized as important drivers of lung injury and repair. We therefore performed a bibliometric analysis to map research trends, key contributors, and evolving hotspots in macrophage-related BPD research.
METHODS: We searched the Web of Science Core Collection (WoSCC) on December 5, 2025, using topic terms for BPD/ventilator-induced lung injury and macrophage-related keywords, and included English-language original research articles published from January 1990 to December 2025. VOSviewer, CiteSpace, and the R package bibliometrix were used to analyze publication trends, collaboration networks, keyword co-occurrence clusters, and burst keywords.
RESULTS: A total of 587 original research articles from 1990 to 2025 were included. Annual publications rose from fewer than 5 before 1995 to a peak of 30 in 2020, showing steady linear growth. The USA led in output (217 articles, 37.0%), followed by China (123, 21.0%) and Germany (45, 7.7%). The University of Toronto (104 articles) and Harvard University (78 articles) were the most productive institutions. The top journal was American Journal of Physiology-Lung Cellular and Molecular Physiology (70 articles, h-index =37). Leading authors included Li Li-Fu (11 articles) and Jankov Robert P. (10 articles). Keyword network and temporal analyses revealed a thematic shift from early emphasis on ventilator-associated injury and classical inflammatory mediators toward developmental biology, gene regulation, cellular heterogeneity, and pulmonary vascular disease, with recent bursts highlighting NF-κB signaling, pulmonary hypertension, inflammation, and BPD.
CONCLUSIONS: Macrophage-related BPD research has shifted from early work on general inflammation and injury to more recent studies emphasizing gene regulation, signaling pathways, and pulmonary vascular complications. Key needs include stronger integration of human data with animal models, improved data standardization, and broader collaboration. Future studies should combine multi-omics with clinical outcomes to support immune-targeted and precision approaches for neonatal lung disease.