Evidence map›Paper›PMID 36860872›Full record

ReviewFrontiers in immunology2023

Chemokines and chemokine receptors as promising targets in rheumatoid arthritis.

Masanori A Murayama, Jun Shimizu, Chie Miyabe, Kazuo Yudo, Yoshishige Miyabe

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
17.0field-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

39 citing papers in PubMed, 74 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Targeting CXCR1/2 suppresses TThe journal of allergy and clinical immunology. Global · 2026
    Article
  5. Monocyte Migration Emerges from a Divergent Chemokine Signaling Network.bioRxiv : the preprint server for biology · 2026
    Article
  6. Review
  7. Article
  8. Article
  9. CD4Nature medicine · 2026
    Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Review
  15. Article
  16. Synovial MS4A4A correlates with inflammation and counteracts response to corticosteroids in arthritis.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  17. Article
  18. Core-Shell ZnOACS applied materials & interfaces · 2025
    Article
  19. Unveiling the crucial role of CD8Journal of translational autoimmunity · 2025
    Article
  20. 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

5 authors at 2 institutions in 1 country.

Masanori A MurayamaDepartment of Animal Models for Human Diseases, Institute of Biomedical Science, Kansai Medical University, Osaka, Japan.
Jun ShimizuDepartment of Immunology and Medicine, St. Marianna University School of Medicine, Kanagawa, Japan.
Chie MiyabeDepartment of Frontier Medicine, Institute of Medical Science, St. Marianna University School of Medicine, Kanagawa, Japan.
Kazuo YudoDepartment of Frontier Medicine, Institute of Medical Science, St. Marianna University School of Medicine, Kanagawa, Japan.
Yoshishige MiyabeDepartment of Immunology and Medicine, St. Marianna University School of Medicine, Kanagawa, Japan.
St. Marianna University School of Medicine · JPKansai Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rheumatoid arthritis (RA) is an autoimmune disease that commonly causes inflammation and bone destruction in multiple joints. Inflammatory cytokines, such as IL-6 and TNF-α, play important roles in RA development and pathogenesis. Biological therapies targeting these cytokines have revolutionized RA therapy. However, approximately 50% of the patients are non-responders to these therapies. Therefore, there is an ongoing need to identify new therapeutic targets and therapies for patients with RA. In this review, we focus on the pathogenic roles of chemokines and their G-protein-coupled receptors (GPCRs) in RA. Inflamed tissues in RA, such as the synovium, highly express various chemokines to promote leukocyte migration, tightly controlled by chemokine ligand-receptor interactions. Because the inhibition of these signaling pathways results in inflammatory response regulation, chemokines and their receptors could be promising targets for RA therapy. The blockade of various chemokines and/or their receptors has yielded prospective results in preclinical trials using animal models of inflammatory arthritis. However, some of these strategies have failed in clinical trials. Nonetheless, some blockades showed promising results in early-phase clinical trials, suggesting that chemokine ligand-receptor interactions remain a promising therapeutic target for RA and other autoimmune diseases.

Indexed as

Arthritis, RheumatoidAutoimmune DiseasesAnimalsChemokinesCytokinesLigandsProspective StudiesReceptors, ChemokineChemokinesCytokinesLigandsReceptors, Chemokineblockadechemokinechemokine receptorleukocytemigrationrheumatoid arthritis

Identifiers

PMID36860872
PMCPMC9968812
OpenAlexW4320495273

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.