ArticleNature communications2026
Microbiota-derived IPA protects against colitis by regulating intestinal HMGCS2-mediated ketogenesis to facilitate mucosal healing.
Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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.
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Who cites it
5 citing papers in PubMed.
- ROS-responsive small-molecule self-assembled nanocarrier-integrated hydrogels for ulcerative colitis treatment.Materials today. Bio · 2026Article
- Microbiota-Associated Amino Acid Metabolites in Inflammatory Bowel Disease: Emerging Key Players in the Host-Microbe Interface.Microorganisms · 2026Review
- Integrating host-microbiota metabolic networks: how aromatic amino acids shape immune homeostasis and affect disease progression.Cellular & molecular immunology · 2026Review
- A microbiota-IPA axis facilitates intestinal stem cell-mediated regeneration in colitis through a Hopx-associated program.Nature communications · 2026Article
- Gut microbiota-derived metabolites target C5AR1/KDM2A/HCAR3 axis in inflammatory bowel disease: a multi-machine learning algorithms and molecular docking study.Frontiers in cellular and infection microbiology · 2026Article
Corrections and comments
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Authors and funding
19 authors.
Funding
Abstract
The gut microbiota sustains intestinal homeostasis, yet how microbial metabolites direct epithelial repair remains unclear. Here we identify indole-3-propionic acid (IPA), a tryptophan-derived bacterial metabolite, as a key regulator of mucosal healing. IPA activates PPARα in intestinal epithelial cells, enhancing transcription of the ketogenic enzyme HMGCS2 and boosting β‑hydroxybutyrate (BHB) production. BHB in turn stimulates LGR5⁺ intestinal stem cells, accelerating epithelial regeneration. Using germ-free models and the IPA‑producer Peptostreptococcus russellii, we show that dietary tryptophan and specific commensals sustain luminal IPA levels, which are critical for recovery in colitis. Restoration of IPA or BHB attenuates inflammation and barrier defects, outlining a microbiota‑metabolite‑stem cell axis that could be therapeutically targeted in inflammatory bowel disease and other barrier disorders.
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Registered trials
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