Evidence map›Paper›PMID 37860753›Full record

ArticleiScience2023

Epigenetic and transcriptional regulation of CCL17 production by glucocorticoids in arthritis.

Tanya J Lupancu, Kevin M C Lee, Mahtab Eivazitork, Cecil Hor, Andrew J Fleetwood, Andrew D Cook, Moshe Olshansky, Stephen J Turner, Richard de Steiger, Keith Lim and 2 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in iScience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.8field-weighted citation impact, top 24% 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

3 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Article
  3. 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

12 authors at 3 institutions in 1 country.

Tanya J LupancuDepartment of Medicine, Royal Melbourne Hospital, The University of Melbourne, Parkville, VIC 3052, Australia.
Kevin M C LeeDepartment of Medicine, Royal Melbourne Hospital, The University of Melbourne, Parkville, VIC 3052, Australia.
Mahtab EivazitorkDepartment of Medicine, Royal Melbourne Hospital, The University of Melbourne, Parkville, VIC 3052, Australia.
Cecil HorDepartment of Medicine, Western Health, The University of Melbourne, St Albans, VIC 3021, Australia.
Andrew J FleetwoodDepartment of Medicine, Royal Melbourne Hospital, The University of Melbourne, Parkville, VIC 3052, Australia.
Andrew D CookDepartment of Medicine, Royal Melbourne Hospital, The University of Melbourne, Parkville, VIC 3052, Australia.
Moshe OlshanskyDepartment of Microbiology, Monash University, Clayton, VIC 3800, Australia.
Stephen J TurnerDepartment of Microbiology, Monash University, Clayton, VIC 3800, Australia.
Richard de SteigerDepartment of Surgery, Epworth HealthCare, The University of Melbourne, Richmond, VIC 3121, Australia.
Keith LimDepartment of Medicine, Western Health, The University of Melbourne, St Albans, VIC 3021, Australia.
John A HamiltonDepartment of Medicine, Royal Melbourne Hospital, The University of Melbourne, Parkville, VIC 3052, Australia.
Adrian A AchuthanDepartment of Medicine, Royal Melbourne Hospital, The University of Melbourne, Parkville, VIC 3052, Australia.
The Royal Melbourne Hospital · AUThe University of Melbourne · AUMonash University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glucocorticoids (GCs) are potent anti-inflammatory agents and are broadly used in treating rheumatoid arthritis (RA) patients, albeit with adverse side effects associated with long-term usage. The negative consequences of GC therapy provide an impetus for research into gaining insights into the molecular mechanisms of GC action. We have previously reported that granulocyte-macrophage colony-stimulating factor (GM-CSF)-induced CCL17 has a non-redundant role in inflammatory arthritis. Here, we provide molecular evidence that GCs can suppress GM-CSF-mediated upregulation of IRF4 and CCL17 expression via downregulating JMJD3 expression and activity. In mouse models of inflammatory arthritis, GC treatment inhibited CCL17 expression and ameliorated arthritic pain-like behavior and disease. Significantly, GC treatment of RA patient peripheral blood mononuclear cells

Indexed as

EpigeneticsMolecular mechanism of gene regulationOrthopedics

Identifiers

PMID37860753
PMCPMC10583050
OpenAlexW4387095179

What OpenQuestion 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 OpenQuestion graph.