Evidence map›Paper›PMID 37402858›Full record

ArticleScientific reports2023

IRAK3-mediated suppression of pro-inflammatory MyD88/IRAK signaling affects disease severity in acute pancreatitis.

Franziska G Thiel, Saeedeh Asgarbeik, Juliane Glaubitz, Anika Wilden, Markus M Lerch, Frank Ulrich Weiss, Matthias Sendler

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
9.8field-weighted citation impact, top 1% 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

10 citing papers in PubMed, 29 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Franziska G ThielDepartment of Medicine A, University Medicine, University of Greifswald, Fleischmannstr. 41, 17475, Greifswald, Germany.
Saeedeh AsgarbeikDepartment of Medicine A, University Medicine, University of Greifswald, Fleischmannstr. 41, 17475, Greifswald, Germany.
Juliane GlaubitzDepartment of Medicine A, University Medicine, University of Greifswald, Fleischmannstr. 41, 17475, Greifswald, Germany.
Anika WildenDepartment of Medicine A, University Medicine, University of Greifswald, Fleischmannstr. 41, 17475, Greifswald, Germany.
Markus M LerchDepartment of Medicine A, University Medicine, University of Greifswald, Fleischmannstr. 41, 17475, Greifswald, Germany.
Frank Ulrich WeissDepartment of Medicine A, University Medicine, University of Greifswald, Fleischmannstr. 41, 17475, Greifswald, Germany.
Matthias SendlerDepartment of Medicine A, University Medicine, University of Greifswald, Fleischmannstr. 41, 17475, Greifswald, Germany. matthias.sendler@uni-greifswald.de.
Universitätsmedizin Greifswald · DEUniversität Greifswald · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute pancreatitis (AP), which is characterized by self-digestion of the pancreas by its own prematurely activated digestive proteases, is a major reason for hospitalization. The autodigestive process causes necrotic cell death of pancreatic acinar cells and the release of damage associated molecular pattern which activate macrophages and drive the secretion of pro-inflammatory cytokines. The MYD88/IRAK signaling pathway plays an important role for the induction of inflammatory responses. Interleukin-1 receptor associated kinase-3 (IRAK3) is a counter-regulator of this pathway. In this study, we investigated the role of MYD88/IRAK using Irak3-/- mice in two experimental animal models of mild and severe AP. IRAK3 is expressed in macrophages as well as pancreatic acinar cells where it restrains NFκB activation. Deletion of IRAK3 enhanced the migration of CCR2

Indexed as

PancreatitisAcute DiseaseAdaptor Proteins, Signal TransducingAnimalsCeruletideDisease Models, AnimalInflammationInterleukin-1 Receptor-Associated KinasesMiceMice, Inbred C57BLMyeloid Differentiation Factor 88NecrosisPancreasPatient AcuitySignal TransductionSystemic Inflammatory Response SyndromeAdaptor Proteins, Signal TransducingCeruletideInterleukin-1 Receptor-Associated KinasesIrak3 protein, mouseMyeloid Differentiation Factor 88

Identifiers

PMID37402858
PMCPMC10319718
OpenAlexW4383100985

What OpenQuestion holds

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Registered trials

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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.