ArticleNature communications2024
Xenotransplanted human organoids identify transepithelial zinc transport as a key mediator of intestinal adaptation.
Article in Nature communications, 2024. 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.
- Iron and Other Metal Ions in Human Health and Disease.MedComm · 2026Review
- Biological Insights into Intestinal Adaptation from Preclinical Models of Short Bowel Syndrome.Cells · 2026Review
- Advances in vascularized organoids.Chinese medical journal · 2026Review
- Review
- Molecular Mechanisms of Intestinal Adaptation in Short Bowel Syndrome: A Comprehensive Review.International journal of molecular sciences · 2026Review
- Enteric nervous system as a therapeutic target in gastrointestinal disorders.World journal of gastrointestinal pharmacology and therapeutics · 2025Article
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Authors and funding
22 authors.
Funding
Abstract
Short bowel syndrome (SBS) leads to severe morbidity and mortality. Intestinal adaptation is crucial in improving outcomes. To understand the human gene pathways associated with adaptation, we perform single-cell transcriptomic analysis of human small intestinal organoids explanted from mice with experimental SBS. We show that transmembrane ion pathways, specifically the transepithelial zinc transport pathway genes SLC39A4 and SLC39A5, are upregulated in SBS. This discovery is corroborated by an external dataset, bulk RT-qPCR, and Western blots. Oral zinc supplementation is shown to improve survival and weight gain of SBS mice and increase the proliferation of intestinal crypt cells in vitro. Finally, we identify the upregulation of SLC39A5 and associated transcription factor KLF5 in biopsied intestinal tissue specimens from patients with SBS. Thus, we identify zinc supplementation as a potential therapy for SBS and describe a xenotransplantation model that provides a platform for discovery in other intestinal diseases.
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