ArticleNPJ biofilms and microbiomes2025
Clostridium scindens attenuates acute kidney injury by producing indole-3-acetic acid.
Article in NPJ biofilms and microbiomes, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Renoprotective effects of gut NHE3 inhibitor tenapanor in a rat model of unilateral renal ischemia-reperfusion injury with contralateral nephrectomy.Biochemistry and biophysics reports · 2026Article
- Bile Acids and the Gut-X Axis: TCM-Mediated Systemic Protection and Therapeutic Opportunities for Multi-Organ Diseases.Metabolites · 2026Review
- Towards microbiome-informed strategies for predicting and preventing pregnancy complications.Reproduction & fertility · 2026Review
- Multi-omics analysis reveals the critical role of gut microbiota related tryptophan and glutathione metabolism in sepsis-associated encephalopathy.BMC microbiology · 2026Article
- Microbiota-associated metabolic networks in gut-kidney communication and renal immune regulation: mechanisms and therapeutic potential.Frontiers in microbiology · 2026Review
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Authors and funding
8 authors.
Funding
Abstract
The association between gut microbiota and acute kidney injury (AKI) has garnered increased attention recently. Herein, we investigated the effect of the gut microbiota and its metabolites on regulating AKI-associated kidney injury and inflammation. We observed that Clostridium scindens (CS) can ameliorate ischemia/reperfusion injury/folic acid-induced renal dysfunction, oxidative stress, and inflammation, and enhance intestinal barrier function. Mechanistically, CS can facilitate indole-3-acetic acid (IAA) production via the tryptophan metabolic pathway: tryptophan-indole-3-pyruvic acid-IAA. The increased intestinal IAA activates the aryl hydrocarbon receptor to restore intestinal barrier integrity and decreases interferon-γ influx into the bloodstream, thereby alleviating renal inflammation. The natural product Nobiletin ameliorated AKI by promoting CS growth. Our findings suggest that regulating CS is a promising approach for treating AKI.
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