ReviewJournal of inflammation research2026
Microplastics, Gut Dysbiosis, and Inflammatory Pathways in Ulcerative Colitis.
Review in Journal of inflammation research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Microplastics (MPs) are pervasive environmental pollutants characterized by their widespread distribution. They can enter the human body through multiple routes, including inhalation and dietary intake, accumulate in the gastrointestinal tract, and subsequently disrupt intestinal microecological homeostasis, thereby contributing to digestive diseases. Ulcerative colitis (UC), a chronic inflammatory bowel disease of unclear etiology, has been closely associated with gut microbiota dysbiosis, which is considered one of its central pathogenic mechanisms. This review comprehensively review the fundamental characteristics of MPs and their interactions with the gut microbiota and microbial metabolites. It further elucidates the key mechanisms by which MPs mediate the initiation and progression of UC, with particular emphasis on intestinal mucosal barrier dysfunction and immune dysregulation. Mechanistically, MPs disrupt SCFAs-producing microbial networks and activate epithelial inflammatory pathways, particularly TLR4-NF-κB signaling, thereby amplifying mucosal inflammation in UC. This review is the first to completely connect the regulatory axis of MPs - gut microbiota - metabolites - intestinal barrier - immune inflammation, clarify the core pathological chain of UC induced by MPs, make up for the shortcomings of existing reviews that only conduct single-dimensional analysis and lack integration of complete mechanisms, and provide a new theoretical framework for this field. Additionally, current research limitations are discussed, and future research directions and potential intervention strategies are proposed, aiming to provide novel theoretical insights into the etiology and prevention of UC.
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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 OpenQuestion graph.