ArticleInflammatory bowel diseases2014
Genetic deletion of Klf4 in the mouse intestinal epithelium ameliorates dextran sodium sulfate-induced colitis by modulating the NF-κB pathway inflammatory response.
Article in Inflammatory bowel diseases, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 45 citations in OpenAlex.
- Krüppel-like factor 4 acts as a potential therapeutic target of Sijunzi decoction for treatment of colorectal cancer.Cancer gene therapy · 2017Trial
- Regulation of Inducible Nitric Oxide Synthase (NOS2) Expression in Healthy and Inflamed Bowel: A Narrative Review.International journal of molecular sciences · 2026Review
- The Mechanism of KLF4-Mediated NF-κB/NLRP3 Pathway Regulating Arteriovenous Fistula Dysfunction.Acta Cardiologica Sinica · 2026Article
- Review
- KLF feedback loops in innate immunity.Frontiers in immunology · 2025Review
- The protective effect of iron isomaltoside on myocardial ischemia-reperfusion injury via the suppression of KLF4/NF-κB signaling.PloS one · 2025Article
- Downregulated KLF4, induced by m6A modification, aggravates intestinal barrier dysfunction in inflammatory bowel disease.Cellular and molecular life sciences : CMLS · 2024Article
- KLF4 interacts with TXNIP to modulate the pyroptosis in ulcerative colitis via regulating NLRP3 signaling.Immunity, inflammation and disease · 2024Article
- Fecal Microbiota Restoration Modulates the Microbiome in Inflammation-Driven Colorectal Cancer.Cancers · 2023Article
- Nucleic acid strategies for infectious disease treatments: The nanoparticle-based oral delivery route.Frontiers in pharmacology · 2022Review
- Agent Clustering Strategy Based on Metabolic Flux Distribution and Transcriptome Expression for Novel Drug Development.Biomedicines · 2021Article
- ATF4-mediated histone deacetylase HDAC1 promotes the progression of acute pancreatitis.Cell death & disease · 2021Article
- MicroRNA-21 from bone marrow mesenchymal stem cell-derived extracellular vesicles targets TET1 to suppress KLF4 and alleviate rheumatoid arthritis.Therapeutic advances in chronic disease · 2021Article
- A Novel PAK1-Notch1 Axis Regulates Crypt Homeostasis in Intestinal Inflammation.Cellular and molecular gastroenterology and hepatology · 2021Article
- Recent Discoveries on the Involvement of Krüppel-Like Factor 4 in the Most Common Cancer Types.International journal of molecular sciences · 2020Review
- KLF4 activates NFκB signaling and esophageal epithelial inflammation via the Rho-related GTP-binding protein RHOF.PloS one · 2019Article
- Increased Genetic Instability and Accelerated Progression of Colitis-Associated Colorectal Cancer through Intestinal Epithelium-specific Deletion ofMolecular cancer research : MCR · 2019Article
- Subcutaneously administered adrenomedullin exerts a potent therapeutic effect in a murine model of ulcerative colitis.Human cell · 2019Article
- Synbiotics suppress colitis-induced tumorigenesis in a colon-specific cancer mouse model.PloS one · 2019Article
- Loss of the Krüppel-like factor 4 tumor suppressor is associated with epithelial-mesenchymal transition in colorectal cancer.Journal of cancer metastasis and treatment · 2019Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundKrüppel-like factor 4 (KLF4) is a zinc finger transcription factor expressed in the differentiated epithelial cells lining of the intestine. Under physiological conditions, KLF4 inhibits cell proliferation. Conversely, KLF4 mediates proinflammatory signaling in macrophages and its overexpression in the esophageal epithelium activates cytokines, leading to inflammation-mediated esophageal squamous cell cancer formation in mice. Here, we tested whether KLF4 has a proinflammatory activity in experimental colitis in mice.
methodsVillin-Cre;Klf4 mice with intestine-specific Klf4 deletion (Klf4) and control mice with floxed Klf4 gene (Klf4) were treated or not with 3% dextran sodium sulfate (DSS) for 7 days to induce colitis. Additionally, WT mice were administered or not, nanoparticles loaded with scrambled or Klf4-siRNA, and concomitantly given DSS.
resultsCompared with DSS-treated Klf4 mice, DSS-treated Klf4 mice were significantly less sensitive to DSS-induced colitis. DSS treatment of Klf4 mice induced Klf4 expression in the crypt zone of the colonic epithelium. DSS-treated Klf4 mice had increased proliferation relative to DSS-treated control mice. DSS treatment induced NF-κB signaling pathway in Klf4 mice colon but not Klf4 mice. Additionally, WT mice given DSS and nanoparticle/Klf4-siRNA were less sensitive to colitis and had reduced Klf4 expression and while maintaining the proliferative response in the colonic epithelium.
conclusionsOur results indicate that Klf4 is an important mediator of DSS-induced colonic inflammation by modulating NF-κB signaling pathway and could be involved in the pathogenesis and/or propagation of inflammatory bowel disease. Thus, Klf4 may represent a novel therapeutic target in inflammatory bowel disease.
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