ArticleiScience2025
Disruption of the transsulfuration pathway by acute kidney injury causes intestinal damage.
Article in iScience, 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.
- Amino Acid Metabolism in Health and Disease.MedComm · 2026Review
- Analysis of the Spatiotemporal Digestion Characteristics of Pine Pollen Processed by Different Methods in Middle-Aged Adults Using an In Vitro Digestion Model System.Foods (Basel, Switzerland) · 2026Article
- Sulfur-Containing Amino Acids: The Conversion Process from Product to Substrate.International journal of molecular sciences · 2026Review
- Gut microbial-derived metabolites: key players in kidney disease and renal fibrosis.International journal of biological sciences · 2026Review
- Gut microbiota in Henoch-Schönlein purpura: from pathogenesis to therapeutic strategies.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute kidney injury (AKI) impairs intestinal function through oxidative stress. The transsulfuration pathway is essential for sulfur amino acid metabolism and antioxidant defense through glutathione biosynthesis. This study investigated how AKI caused intestinal injury and the mechanisms involved. AKI was induced in Sprague-Dawley rats through kidney ischemia (45 min)-reperfusion (24 h). AKI decreased intestinal glutathione (antioxidant) levels and compromised intestinal barrier function. Glutathione biosynthesis in mammals requires cysteine made through the reverse transsulfuration pathway, catalyzed by cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CSE). AKI decreased the expression of these enzymes in intestinal epithelium. AKI also altered gut microbiota composition and the expression of bacterial enzymes in the forward transsulfuration pathway, which could disrupt intestinal antioxidant defense. The inhibition of this pathway in gut epithelial cells reduced glutathione levels and tight junction protein expression. These results suggest that the disruption of the transsulfuration pathway impairs antioxidant defense, leading to intestinal barrier damage and dysbiosis in AKI.
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Registered trials
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