Metabolic dysfunction, antidiabetic drugs, and asthma: bibliometric evidence, emerging trends, and translational
Rong Jiang1, Jie Wang2, Siping Wang3
1Department of Nursing, Yantaishan Hospital, Yantai, Shandong, China.
Background:
The association among metabolic dysfunction, antidiabetic drugs, and asthma has attracted increasing attention in recent years. However, the knowledge structure, dominant metabolic mechanisms, drug-related research hotspots, and clinical translational evidence in this interdisciplinary field remain insufficiently characterized.
Methods:
This study conducted a bibliometric evidence-mapping and visualization analysis of research linking metabolic dysfunction, antidiabetic drugs, and asthma published between 2006 and 2025. Data were obtained from the Web of Science Core Collection, Scopus, and PubMed. Bibliometric and visualization methods were used to identify global research trends, major knowledge domains, thematic evolution, and emerging translational frontiers.
Results:
A total of 1, 502 records from the Web of Science Core Collection, 6, 710 records from Scopus, and 38 PubMed-indexed clinical studies were included. Publication output showed an overall upward trend, with a marked increase in research attention after 2015. Keyword and clustering analyses indicated that obesity, insulin resistance, metabolic syndrome, inflammation, oxidative stress, adipokines, lung function, and airway hyperresponsiveness formed the dominant knowledge base of this field. In contrast, drug-related topics, including metformin, peroxisome proliferator-activated receptor γ agonists, glucagon-like peptide-1 receptor agonists, sodium-glucose cotransporter 2 inhibitors, and dipeptidyl peptidase-4 inhibitors, gradually entered the research network but generally showed relatively limited centrality and uneven clinical evidence. Reference co-citation and burst analyses further suggested that recent research frontiers are shifting toward drug-related mechanisms, asthma exacerbations, and clinical outcome evaluation.
Conclusion:
Research in this field has evolved from early studies of metabolic comorbidity and inflammatory mechanisms toward drug-related mechanisms, asthma outcomes, and translational evidence. The dominant knowledge base is centered on obesity, insulin resistance, metabolic inflammation, oxidative stress, and airway dysfunction, whereas drug-specific evidence remains emerging and uneven across drug classes. Future studies should integrate large-scale clinical data, prospective cohorts, and randomized controlled trials to clarify whether selected antidiabetic drugs may modify asthma outcomes in metabolically defined asthma phenotypes. This study provides an evidence-mapping perspective for understanding the metabolic, pharmacological, and clinical translational links among metabolic dysfunction, antidiabetic drugs, and asthma.
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