Evidence map›Paper›PMID 30320600›Full record

ArticleThe Journal of clinical investigation2018

Thirty-eight-negative kinase 1 mediates trauma-induced intestinal injury and multi-organ failure.

Milena Armacki, Anna Katharina Trugenberger, Ann K Ellwanger, Tim Eiseler, Christiane Schwerdt, Lucas Bettac, Dominik Langgartner, Ninel Azoitei, Rebecca Halbgebauer, Rüdiger Groß and 24 more

Open access · bronzeAbstract read
In one paragraph

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 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
1.7field-weighted citation impact, top 15% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

32 citing papers in PubMed, 75 citations in OpenAlex.

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  14. Trauma-toxicology: concepts, causes, complications.Naunyn-Schmiedeberg's archives of pharmacology · 2024
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

34 authors at 9 institutions in 2 countries.

Milena ArmackiDepartment of Internal Medicine I, University Hospital Ulm, Ulm, Germany.
Anna Katharina TrugenbergerDepartment of Internal Medicine I, University Hospital Ulm, Ulm, Germany.
Ann K EllwangerDepartment of Internal Medicine I, University Hospital Ulm, Ulm, Germany.
Tim EiselerDepartment of Internal Medicine I, University Hospital Ulm, Ulm, Germany.
Christiane SchwerdtWaldkrankenhaus "Rudolph Elle" Eisenberg, Lehrstuhl für Orthopädie Uniklinik Jena, Jena, Germany.
Lucas BettacDepartment of Internal Medicine I, University Hospital Ulm, Ulm, Germany.
Dominik LanggartnerLaboratory for Molecular Psychosomatics, Clinic for Psychosomatic Medicine and Psychotherapy, and.
Ninel AzoiteiDepartment of Internal Medicine I, University Hospital Ulm, Ulm, Germany.
Rebecca HalbgebauerInstitute of Clinical and Experimental Trauma Immunology, University Hospital Ulm, Ulm, Germany.
Rüdiger GroßDepartment of Internal Medicine I, University Hospital Ulm, Ulm, Germany.
Tabea BarthDepartment of Internal Medicine I, University Hospital Ulm, Ulm, Germany.
André LechelDepartment of Internal Medicine I, University Hospital Ulm, Ulm, Germany.
Benjamin M WalterDepartment of Internal Medicine I, University Hospital Ulm, Ulm, Germany.
Johann M KrausInstitute of Medical Systems Biology and.
Christoph WiegreffeInstitute of Molecular and Cellular Anatomy, Ulm University, Ulm, Germany.
Johannes GrimmInstitute of Pathology and.
Annika ScheffoldDepartment of Internal Medicine III, University Hospital Ulm, Ulm, Germany.
Marlon R SchneiderGene Center, LMU Munich, Munich, Germany.
Kenneth PeukerCenter for Regenerative Therapies Dresden, TU Dresden, Dresden, Germany.
Sebastian ZeißigCenter for Regenerative Therapies Dresden, TU Dresden, Dresden, Germany.
Stefan BritschInstitute of Molecular and Cellular Anatomy, Ulm University, Ulm, Germany.
Stefan Rose-JohnInstitute of Biochemistry, CA University Kiel, Kiel, Germany.
Sabine VettorazziInstitute of Comparative Molecular Endocrinology, Ulm University, Ulm, Germany.
Eckhart WolfGene Center, LMU Munich, Munich, Germany.
Andrea TannapfelInstitute of Pathology, Ruhr University Bochum, Bochum, Germany.
Konrad SteinestelInstitute of Pathology and Molecular Pathology, Bundeswehrkrankenhaus Ulm, Ulm, Germany.
Stefan O ReberLaboratory for Molecular Psychosomatics, Clinic for Psychosomatic Medicine and Psychotherapy, and.
Paul WaltherCentral Facility for Electron Microscopy, University of Ulm, Ulm, Germany.
Hans A KestlerInstitute of Medical Systems Biology and.
Peter RadermacherInstitute of Anesthesiological Pathophysiology and Process Engineering, Ulm University, Ulm, Germany.
Thomas Fe BarthInstitute of Pathology and.
Markus Huber-LangInstitute of Clinical and Experimental Trauma Immunology, University Hospital Ulm, Ulm, Germany.
Alexander KlegerDepartment of Internal Medicine I, University Hospital Ulm, Ulm, Germany.
Thomas SeufferleinDepartment of Internal Medicine I, University Hospital Ulm, Ulm, Germany.
University Hospital Ulm · DEUniversität Ulm · DEInstitute of Medical Biology · SGLudwig-Maximilians-Universität München · DETechnische Universität Dresden · DEBundeswehrkrankenhaus · DEHochschule für Angewandte Wissenschaften Kiel · DERuhr University Bochum · DEWaldkrankenhaus Rudolf Elle · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dysregulated intestinal epithelial apoptosis initiates gut injury, alters the intestinal barrier, and can facilitate bacterial translocation leading to a systemic inflammatory response syndrome (SIRS) and/or multi-organ dysfunction syndrome (MODS). A variety of gastrointestinal disorders, including inflammatory bowel disease, have been linked to intestinal apoptosis. Similarly, intestinal hyperpermeability and gut failure occur in critically ill patients, putting the gut at the center of SIRS pathology. Regulation of apoptosis and immune-modulatory functions have been ascribed to Thirty-eight-negative kinase 1 (TNK1), whose activity is regulated merely by expression. We investigated the effect of TNK1 on intestinal integrity and its role in MODS. TNK1 expression induced crypt-specific apoptosis, leading to bacterial translocation, subsequent septic shock, and early death. Mechanistically, TNK1 expression in vivo resulted in STAT3 phosphorylation, nuclear translocation of p65, and release of IL-6 and TNF-α. A TNF-α neutralizing antibody partially blocked development of intestinal damage. Conversely, gut-specific deletion of TNK1 protected the intestinal mucosa from experimental colitis and prevented cytokine release in the gut. Finally, TNK1 was found to be deregulated in the gut in murine and porcine trauma models and human inflammatory bowel disease. Thus, TNK1 might be a target during MODS to prevent damage in several organs, notably the gut.

Indexed as

AnimalsDisease Models, AnimalFemaleFetal ProteinsInflammatory Bowel DiseasesInterleukin-6IntestinesMiceMultiple Organ FailureMultiple TraumaProtein-Tyrosine KinasesSTAT3 Transcription FactorSwineSystemic Inflammatory Response SyndromeTranscription Factor RelATumor Necrosis Factor-alphaFetal ProteinsIL6 protein, humanInterleukin-6interleukin-6, mouseKos1 protein, mouseProtein-Tyrosine KinasesRELA protein, humanRela protein, mouseSTAT3 protein, humanStat3 protein, mouseSTAT3 Transcription FactorTNK1 protein, humanTranscription Factor RelATumor Necrosis Factor-alphaApoptosisGastroenterologyInflammationInflammatory bowel diseaseTight junctions

Identifiers

PMID30320600
PMCPMC6205400
OpenAlexW2896959233

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.