ReviewPflugers Archiv : European journal of physiology2017
Active and passive involvement of claudins in the pathophysiology of intestinal inflammatory diseases.
Review in Pflugers Archiv : European journal of physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04212507 (The Gut-Skin Axis Integrity in Psoriatic Patients), which is not on this map. Cited by 57 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
The Gut-Skin Axis Integrity in Psoriatic Patients
Who cites it
57 citing papers in PubMed, 86 citations in OpenAlex.
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- Effect and Mechanisms of Electroacupuncture on Mucosal Healing in Ulcerative Colitis Mice via Non-neuroronal Cholinergic System.Chinese journal of integrative medicine · 2026Article
- MAIT Cells Maintain Intestinal Homeostasis Through IL-22 in an Experimental Colitis.Journal of inflammation research · 2026Article
- Tight junction dysfunction and cytoskeletal remodeling in Hirschsprung‑associated enterocolitis: A decade of mechanistic insights and therapeutic prospects (Review).Molecular medicine reports · 2026Review
- Proinflammatory cytokines modify CaFrontiers in physiology · 2026Article
- Impaired intestinal permeability in patients with multiple sclerosis.Biomedical papers of the Medical Faculty of the University Palacky, Olomouc, Czechoslovakia · 2025Article
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- Cholecystectomy and the risk of microscopic colitis: a systematic review and meta-analysis.Therapeutic advances in gastroenterology · 2025Article
- (-)-Fenchone Ameliorates TNBS-Induced Colitis in Rats via Antioxidant, Immunomodulatory, and Cytoprotective Mechanisms.Pharmaceuticals (Basel, Switzerland) · 2024Article
- The Role of Claudins in the Pathogenesis of Dextran Sulfate Sodium-Induced Experimental Colitis: The Effects of Nobiletin.Biomolecules · 2024Article
- Lymphocytic colitis can be transcriptionally divided into channelopathic and inflammatory lymphocytic colitis.United European gastroenterology journal · 2024Article
- Colonic Epithelial Permeability to Ions Is Restored after Vedolizumab Treatment and May Predict Clinical Response in Inflammatory Bowel Disease Patients.International journal of molecular sciences · 2024Article
- Micronutrients at Supplemental Levels, Tight Junctions and Epithelial Barrier Function: A Narrative Review.International journal of molecular sciences · 2024Review
- Time-dependent effects of tumor necrosis factor α on CaFrontiers in physiology · 2024Article
- Intestinal Barrier Function and Neurodegenerative Disease.CNS & neurological disorders drug targets · 2024Review
- Amelioration of inflammatory bowel disease byFrontiers in microbiology · 2024Article
- Chronic Stress Exposure Alters the Gut Barrier: Sex-Specific Effects on Microbiota and Jejunum Tight Junctions.Biological psychiatry global open science · 2024Article
- Article
- Mechanism of Acupuncture and Moxibustion on Promoting Mucosal Healing in Ulcerative Colitis.Chinese journal of integrative medicine · 2023Review
- 5-Aminosalicylic acid alters the gut microbiota and altered microbiota transmitted vertically to offspring have protective effects against colitis.Scientific reports · 2023Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intestinal inflammatory diseases, four of which are discussed here, are associated with alterations of claudins. In ulcerative colitis, diarrhea and antigen entry into the mucosa occurs. Claudin-2 is upregulated but data on other claudins are still limited or vary (e.g., claudin-1 and -4). Apart from that, tight junction changes contribute to diarrhea via a leak flux mechanism, while protection against antigen entry disappears behind epithelial gross lesions (erosions) and apoptotic foci. Crohn's disease is additionally characterized by a claudin-5 and claudin-8 reduction which plays an active role in antigen uptake already before gross lesions appear. In microscopic colitis (MC), upregulation of claudin-2 expression is weak and a reduction in claudin-4 may be only passively involved, while sodium malabsorption represents the main diarrheal mechanism. However, claudin-5 is removed from MC tight junctions which may be an active trigger for inflammation through antigen uptake along the so-called leaky gut concept. In celiac disease, primary barrier defects are discussed in the context of candidate genes as PARD3 which regulate cell polarity and tight junctions. The loss of claudin-5 allows small antigens to invade, while the reductions in others like claudin-3 are rather passive events. Taken together, the specific role of single tight junction proteins for the onset and perpetuation of inflammation and the recovery from these diseases is far from being fully understood and is clearly dependent on the stage of the disease, the background of the other tight junction components, the transport activity of the mucosa, and the presence of other barrier features like gross lesions, an orchestral interplay which is discussed in this article.
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