Mapping mitochondria-associated research in inflammatory bowel disease

Background: Mitochondria-associated research has become increasingly prominent in inflammatory bowel disease (IBD), but its publication growth, collaboration structure, knowledge base, and thematic evolution have not been comprehensively quantified. Methods: Web of Science Core Collection records published from 2010 through 2025 were retrieved on September 19, 2025. Of 215 candidate records, 112 met prespecified eligibility criteria. The 111 records with complete Full Record and Cited References metadata were used for primary analyses; 1 additional eligible record was included only in an annual-output sensitivity analysis. Bibliometrix/Biblioshiny, VOSviewer 1.6.20, and R were used for descriptive, network, temporal, and robustness analyses. Results: Annual output increased significantly (Kendall τ = 0.638, P = .0009; Sen slope = 1.20 publications/year, 95% confidence interval 0.50–1.71), whereas annualized citation impact showed no significant monotonic trend after exclusion of 2025 (Spearman ρ = 0.093, P = .742). China led corresponding-author output (39 articles), while the United States had the highest aggregate citation count (985). Multi-country publications accounted for 35 of 111 articles (31.5%). The largest institutional collaboration component contained 53 organizations in 8 clusters, and the author component contained 15 authors in 2 clusters. The primary author-keyword network included 22 terms, 6 clusters, 90 links, and a total link strength of 181. Mitophagy, mitochondrial dynamics, and machine learning were positioned toward the recent end of the temporal spectrum. Cited-source and cited-reference networks were densely interconnected, indicating a shared multidisciplinary knowledge base. Conclusion: Mitochondria-associated IBD research expanded substantially during 2010 to 2025, with concentrated geographic leadership, recurrent but uneven international collaboration, and overlapping themes spanning inflammation, epithelial biology, metabolism, mitochondrial quality control, and host–microbiome interactions. The findings provide a reproducible map of the literature but should not be interpreted as evidence of biological causality or discrete mechanistic pathways.