ArticleFrontiers in microbiology2026
Gut microbiota and ankylosing spondylitis: mechanisms, functional pathways, and research trends.
Article in Frontiers in microbiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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.
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Who cites it
2 citing papers in PubMed.
- Convergent Gut Microbiome Remodeling Across Ischemic Stroke, Myocardial Infarction, and Longevity Reveals a Shared Ecological Signature of Aging and Disease.International journal of molecular sciences · 2026Article
- Research trends in depression associated with gynecologic cancers from 2006 to 2025: a multidatabase bibliometric and visual analysis.Frontiers in oncology · 2026Review
Corrections and comments
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Authors and funding
4 authors.
Funding
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Abstract
Background: Ankylosing spondylitis (AS) is a chronic immune-mediated inflammatory disease in which genetic susceptibility, mucosal immunity, and environmental factors converge. Growing evidence indicates that gut microbiota dysbiosis is closely involved in AS pathogenesis, yet the evolution of this research field and the underlying functional mechanisms remain to be systematically clarified. Methods: The study performed an analysis of studies on AS and gut microbiota retrieved from the WOSCC, Scopus, and PubMed. Publication trends, collaboration networks, co-citation patterns, and keyword clusters were analyzed to identify major research themes and emerging hotspots in this field. Results: The analysis revealed a progressive shift from descriptive microbiota profiling to mechanistic and causal investigations. Core research themes included microbial dysbiosis, intestinal barrier dysfunction, mucosal immune activation, microbial metabolites, and key inflammatory pathways. Studies increasingly emphasize functional and pathway-level analysis rather than focusing on individual microbial taxa. Mendelian randomization further strengthened causal inference and highlighted the potential of microbiota-related signatures for disease stratification and therapeutic response. Conclusion: These findings support a disturbed gut-joint axis as a central feature of AS and underscore the role of functional microbial pathways in immune dysregulation. Integrating standardized multi-omics data with causal validation and refined clinical phenotyping may facilitate the identification of actionable microbial targets and advance microbiota-informed precision strategies for AS.
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