ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2025
Polyamines regulate mitochondrial metabolism essential for intestinal epithelial renewal and wound healing.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- AMD1-mediated polyamine metabolism governs tubular repair fate by restraining senescence after kidney injury.Renal failure · 2026Article
- Age-Associated Impairment of Paneth Cells Driven by microRNA-152 Promotes Intestinal Epithelial Vulnerability to Pathological Stress.Aging cell · 2026Article
- Article
- Microbial metabolic memory in inflammatory bowel disease: microbiota-derived metabolites, host-microbe reprogramming, and relapse susceptibility.Frontiers in microbiology · 2026Review
- Mitochondrial transfer: a novel paradigm for wound healing.Burns & trauma · 2026Review
- Bidirectional Crosstalk Between Intestinal Epithelium and Immune Microenvironment in Inflammatory Bowel Disease: Mechanisms and Therapeutic Implications.Journal of inflammation research · 2026Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Homeostasis of the mammalian intestinal epithelium is tightly regulated by multiple factors, including cellular polyamines, but the exact mechanism underlying polyamines in this process remains largely unknown. Mitochondria are the powerhouse of cells and can also function as signaling organelles by releasing metabolic by-products. Here, we determined whether polyamines regulate intestinal epithelial renewal and wound healing by altering mitochondrial activity. Depletion of cellular polyamines by inhibiting ornithine decarboxylase with α-difluoromethylornithine (DFMO) resulted in mitochondrial dysfunction as evidenced by decreases in basal and maximal respiration levels, ATP production, and spare respiration capacity. Polyamine depletion by DFMO also decreased the levels of mitochondria-associated proteins prohibitin 1 and COX-IV. Mitochondrial dysfunction induced by DFMO was associated with an inhibition of intestinal organoid growth and epithelial repair after wounding, and this inhibition was ameliorated by administration of the mitochondrial activator Mito-Tempo or exogenous polyamine putrescine. These results indicate that polyamines are necessary for mitochondrial metabolism, in turn, controlling constant intestinal mucosal growth and epithelial repair after acute injury.
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