ArticleEBioMedicine2024
Intestinal epithelium dysfunctions cause IgA deposition in the kidney glomeruli of intestine-specific Ap1m2-deficient mice.
Article in EBioMedicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Distinct clinicopathological features of IgA nephropathy associated with Crohn's disease: comparison with ulcerative colitis and non-IBD IgA nephropathy.Clinical and experimental nephrology · 2026Article
- The Barrier-Microbiota-Inflammation Axis in Colorectal Cancer: Mechanisms and Emerging Diagnostic & Therapeutic Strategies.Cancers · 2026Review
- Gene modification: Exploring the potential in treating kidney diseases.Pharmacological research · 2026Review
- Microbiota-gut-kidney axis in health and renal disease.International journal of biological sciences · 2026Review
- Development of a Novel 11-Gene Signature Related to Immune Subtypes for FibromyalgiaEndocrine, metabolic & immune disorders drug targets · 2026Article
- Gut-kidney axis in IgA nephropathy: mechanisms linking microbiota dysbiosis to immune dysregulation, Gd-IgA1 generation, and renal injury.Frontiers in immunology · 2026Review
- Endocrine disruptors and male infertility: multi-omics identification of key genes in non-obstructive azoospermia.Journal of assisted reproduction and genetics · 2025Article
- The evolving understanding of systemic mechanisms in organ-specific IgA nephropathy: a focus on gut-kidney crosstalk.Theranostics · 2025Review
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIntestinal epithelial cells (IECs) serve as robust barriers against potentially hostile luminal antigens and commensal microbiota. Epithelial barrier dysfunction enhances intestinal permeability, leading to leaky gut syndrome (LGS) associated with autoimmune and chronic inflammatory disorders. However, a causal relationship between LGS and systemic disorders remains unclear. Ap1m2 encodes clathrin adaptor protein complex 1 subunit mu 2, which facilitates polarized protein trafficking toward the basolateral membrane and contributes to the establishment of epithelial barrier functions.
methodsWe generated IEC-specific Ap1m2-deficient (Ap1m2
findingsAp1m2
interpretationIEC barrier dysfunction and subsequent dysbiosis by AP-1B deficiency provoke IgA deposition in the mouse kidney. Our findings provide experimental evidence of a pathological link between LGS and IgAN.
fundingAMED, AMED-CREST, JSPS Grants-in-Aid for Scientific Research, JST CREST, Fuji Foundation for Protein Research, and Keio University Program for the Advancement of Next Generation Research Projects.
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