ArticleThe Journal of clinical investigation2018
Intestinal hyperpermeability: a gateway to multi-organ failure?
Article in The Journal of clinical investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
31 citing papers in PubMed.
- Thirty-Eight-Negative Kinase 1 Is a Mediator of Acute Kidney Injury in Experimental and Clinical Traumatic Hemorrhagic Shock.Frontiers in immunology · 2020Trial
- Systemic Oxidative Stress and Oxidized Albumin Mediate the Pathogenic Kidney-to-Gut Crosstalk by Disrupting Intestinal Barrier Integrity.Biomolecules · 2026Article
- Targeting the Gut in Sepsis: Therapeutic Potential of Medical Gases.Biomolecules · 2026Review
- A Host-Clinical Integrated Prediction Model for Early Sepsis Risk in Diabetic Patients with Acute Infections: Development and Internal Validation.Journal of inflammation research · 2026Article
- Skin Microbiome, Nanotoxicology, and Regulatory Gaps: Chronic Cosmetic Exposure and Skin Barrier Dysfunction-A Systematic Review.Pharmaceutics · 2025Review
- Tranexamic acid is associated with improved intestinal barrier function in traumatic hemorrhagic shock: A clinical prospective cohort study.Critical care (London, England) · 2025Article
- Cimifugin improves intestinal barrier dysfunction by upregulating SIRT1 to regulate the NRF2/HO-1 signaling pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Parishin Protects Against Sepsis-Induced Intestinal Injury by Modulating the ACSL4/p-Smad3/PGC-1α Pathway: An Integrated Approach of Bioinformatics and Experimental Validation.Journal of inflammation research · 2025Article
- SARS-CoV-2 Infection, Vaccination, and Irritable Bowel Syndrome in Veterans: A Cross-Sectional Study.International journal of gastroenterology (New York, N.Y.) · 2024Article
- Critical illness and the gut microbiome.Intensive care medicine · 2024Article
- Article
- Probiotic Pediococcus pentosaceus restored gossypol-induced intestinal barrier injury by increasing propionate content in Nile tilapia.Journal of animal science and biotechnology · 2024Article
- Malvidin alleviates LPS-induced septic intestinal injury through the nuclear factor erythroid 2-related factor 2/reactive oxygen species/NLRP3 inflammasome pathway.Inflammopharmacology · 2024Article
- The human gut microbiome in critical illness: disruptions, consequences, and therapeutic frontiers.Journal of critical care · 2024Review
- Progress in the study of the correlation between sepsis and intestinal microecology.Frontiers in cellular and infection microbiology · 2024Review
- Melatonin mitigates chemotherapy-induced small intestinal atrophy in rats and reduces cytotoxicity in murine intestinal organoids.PloS one · 2024Article
- Article
- Prediction of prokinetic agents in critically ill patients with feeding intolerance: a prospective observational clinical study.Frontiers in nutrition · 2023Article
- Inhibition of platelet activation suppresses reactive enteric glia and mitigates intestinal barrier dysfunction during sepsis.Molecular medicine (Cambridge, Mass.) · 2022Article
- Inhibition of platelet activation suppresses reactive enteric glia and mitigates intestinal barrier dysfunction during sepsis.Molecular medicine (Cambridge, Mass.) · 2022Article
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In critically ill patients, disruption of intestinal epithelial cell function occurs due to exposure of the epithelium to toxic internal and external inflammatory stimuli, which are key factors that trigger sepsis and multi-organ dysfunction syndrome (MODS). A greater understanding of how trauma and gut failure lead to sepsis and progression to MODS is much needed. In this issue of the JCI, Armacki and colleagues identify mechanisms by which thirty-eight-negative kinase 1 (TNK1) promotes the progression from intestinal apoptosis and gut failure to bacterial translocation, sepsis, and MODS. Moreover, the results of this study suggest TNK1 as a potential therapeutic target to prevent sepsis and MODS.
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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.