ArticleJCI insight2025
The septin cytoskeleton is a regulator of intestinal epithelial barrier integrity and mucosal inflammation.
Article in JCI insight, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Sodium Humate Combined with Low-Dose Cefixime Alleviates Intestinal Injury in ETEC Infection via Inhibition of the TLR4/NF-κB Pathway.Biomolecules · 2026Article
- Sucralose and the Gut-Immune Axis: Emerging Evidence Linking Dysbiosis, Barrier Alterations, and Implications for Colitis and Colorectal Cancer Immunotherapy.Biomedicines · 2026Review
- Therapeutic Potential of Ruberythric Acid in Intestinal Inflammation and Barrier Function Reduction.Preventive nutrition and food science · 2026Article
- Septins buffer actomyosin forces to protect the nucleus from genotoxic mechanical stress.bioRxiv : the preprint server for biology · 2026Article
- Application and prospects of organoid-on-a-chip in research on the intestinal mucosal barrier.Burns & trauma · 2026Review
- Article
- Anillin tunes contractility and regulates barrier function during Rho flare-mediated tight junction remodeling.Molecular biology of the cell · 2025Article
Corrections and comments
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Authors and funding
17 authors.
Funding
Abstract
Intestinal epithelial barrier integrity is essential for human health, and its disruption induces and exacerbates intestinal inflammatory disorders. While the epithelial cytoskeleton is critical for maintaining gut barrier-integrity, the role of septins - a family of GTP-binding, cytoskeletal proteins - is largely unknown. This highlights an important knowledge gap, as dysfunction of septins, and specifically septin 9 (SEPT9), is associated with intestinal pathologies. We determined that SEPT9 localizes to the apical junctions of intestinal epithelial cells (IECs), overlapping with both tight and adherens junctions. IEC-specific ablation of SEPT9 in mice resulted in leaky gut, due to mislocalization of junctional proteins, and increased susceptibility to experimental colitis. Consistently, SEPT9 expression was significantly reduced in intestinal mucosa of patients with inflammatory bowel disease (IBD). Using affinity-purification mass spectrometry, super-resolution imaging, and genetic KO, we determined that SEPT9 interacts with and is necessary to recruit nonmuscle myosin IIC (NMIIC) to the IEC perijunctional actomyosin belt. Loss of NMIIC also caused IEC barrier disruption. In summary, SEPT9 regulates intestinal barrier integrity by supporting the assembly of tight and adherens junctions through NMIIC recruitment to the actomyosin belt. The septin cytoskeleton safeguards the intestinal mucosa during acute inflammation, and its disruption in IBD suggests a loss of this protective function.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.