Evidence map›Paper›PMID 39985685›Full record

ArticleCellular and molecular life sciences : CMLS2025

Inhibition of DYRK1B BY C81 impedes inflammatory processes in leukocytes by reducing STAT3 activity.

Sarah Ciurus, Mohammed A F Elewa, Megan A Palmer, Anne Wolf, Mandy Hector, Dominik C Fuhrmann, Dominique Thomas, Robert Gurke, Martin P Schwalm, Lena Berger and 9 more

Abstract read
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Article
  2. Article
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

19 authors.

Sarah CiurusInstitute of Pharmaceutical Biology, Goethe University Frankfurt, Frankfurt, Germany.
Mohammed A F ElewaInstitute of Biochemistry I, Goethe University Frankfurt, Frankfurt, Germany.
Megan A PalmerInstitute of Biochemistry I, Goethe University Frankfurt, Frankfurt, Germany.
Anne WolfLaboratory for Experimental Immunology of the Eye, Department of Ophthalmology, Faculty of Medicine, University of Cologne, University Hospital Cologne, Cologne, Germany.
Mandy HectorLaboratory for Experimental Immunology of the Eye, Department of Ophthalmology, Faculty of Medicine, University of Cologne, University Hospital Cologne, Cologne, Germany.
Dominik C FuhrmannInstitute of Biochemistry I, Goethe University Frankfurt, Frankfurt, Germany.
Dominique ThomasInstitute of Clinical Pharmacology, Goethe University Frankfurt, Frankfurt, Germany.
Robert GurkeInstitute of Clinical Pharmacology, Goethe University Frankfurt, Frankfurt, Germany.
Martin P SchwalmInstitute of Pharmaceutical Chemistry and Buchmann Institute Molecular Life Sciences, Goethe University Frankfurt, Frankfurt, Germany.
Lena BergerInstitute of Pharmaceutical Chemistry and Buchmann Institute Molecular Life Sciences, Goethe University Frankfurt, Frankfurt, Germany.
Thomas J ZechInstitute of Pharmaceutical Biology, Goethe University Frankfurt, Frankfurt, Germany.
Luisa D BurgersInstitute of Pharmaceutical Biology, Goethe University Frankfurt, Frankfurt, Germany.
Rolf MarschalekInstitute of Pharmaceutical Biology, Goethe University Frankfurt, Frankfurt, Germany.
Gerd GeisslingerInstitute of Clinical Pharmacology, Goethe University Frankfurt, Frankfurt, Germany.
Stefan KnappInstitute of Pharmaceutical Chemistry and Buchmann Institute Molecular Life Sciences, Goethe University Frankfurt, Frankfurt, Germany.
Thomas LangmannLaboratory for Experimental Immunology of the Eye, Department of Ophthalmology, Faculty of Medicine, University of Cologne, University Hospital Cologne, Cologne, Germany.
Franz BracherPharmaceutical Chemistry, Department of Pharmacy, Center for Drug Research, Ludwig-Maximilians-University Munich, Munich, Germany.
Andreas WeigertInstitute of Biochemistry I, Goethe University Frankfurt, Frankfurt, Germany.
Robert FürstInstitute of Pharmaceutical Biology, Goethe University Frankfurt, Frankfurt, Germany. robert.fuerst@cup.lmu.de.ORCID http://orcid.org/0000-0002-9926-7578

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic inflammatory diseases are a significant global burden and are associated with dysregulated resolution of inflammation. Therefore, promoting the process of resolution is a promising therapeutic approach. This study presents the potent anti-inflammatory and pro-resolving effects of a natural product-derived compound called C81. Administration of C81 in a therapeutic window resolved inflammation in the murine imiquimod-induced psoriasis model, and reduced microglial infiltration in a laser-induced choroidal neovascularisation model. Investigations into the underlying mechanisms of C81 identified the DYRK1B/STAT3 axis as a new regulator of inflammatory processes in leukocytes. The inhibition of DYRK1B by C81 resulted in attenuated STAT3 phosphorylation. The depletion of STAT3-regulated gene expression led to the inhibition of leukocyte adhesion and migration due to reduced integrin activation, and in addition to the inhibition of the release of pro-inflammatory mediators such as cytokines and eicosanoids. Importantly, the pro-resolving effects of C81 included the cell type-specific induction of apoptosis in neutrophils and a subsequent increase in efferocytosis. In conclusion, we report the DYRK1B/STAT3 axis as a novel and promising therapeutic target for activating the resolution of inflammation.

Indexed as

Anti-Inflammatory AgentsInflammationLeukocytesProtein Serine-Threonine KinasesProtein-Tyrosine KinasesSTAT3 Transcription FactorAnimalsApoptosisCell AdhesionDisease Models, AnimalDyrk KinasesHumansImiquimodMiceMice, Inbred C57BLNeutrophilsAnti-Inflammatory AgentsDyrk KinasesImiquimodProtein Serine-Threonine KinasesProtein-Tyrosine KinasesSTAT3 Transcription FactorDYRK1B-STAT3 signalingKinase inhibitorLeukocytesNatural productResolution of inflammation

Identifiers

PMID39985685
PMCPMC11846820

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.