Evidence map›Paper›PMID 38783357›Full record

ReviewArthritis research & therapy2024

Targeting pathogenic fibroblast-like synoviocyte subsets in rheumatoid arthritis.

Hongyan Qian, Chaoqiong Deng, Shiju Chen, Xinwei Zhang, Yan He, Jingying Lan, Aodi Wang, Guixiu Shi, Yuan Liu

Abstract readReview
In one paragraph

Review in Arthritis research & therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing 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

34 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Review
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

9 authors.

Hongyan Qian *Department of Rheumatology and Clinical Immunology, the First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, 55th, Zhenhai Road, Xiamen, XM, 361000, China.
Chaoqiong Deng *Department of Rheumatology and Clinical Immunology, the First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, 55th, Zhenhai Road, Xiamen, XM, 361000, China.
Shiju ChenDepartment of Rheumatology and Clinical Immunology, the First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, 55th, Zhenhai Road, Xiamen, XM, 361000, China.
Xinwei ZhangDepartment of Rheumatology and Clinical Immunology, the First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, 55th, Zhenhai Road, Xiamen, XM, 361000, China.
Yan HeDepartment of Rheumatology and Clinical Immunology, the First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, 55th, Zhenhai Road, Xiamen, XM, 361000, China.
Jingying LanDepartment of Rheumatology and Clinical Immunology, the First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, 55th, Zhenhai Road, Xiamen, XM, 361000, China.
Aodi WangDepartment of Rheumatology and Clinical Immunology, the First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, 55th, Zhenhai Road, Xiamen, XM, 361000, China.
Guixiu ShiDepartment of Rheumatology and Clinical Immunology, the First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, 55th, Zhenhai Road, Xiamen, XM, 361000, China. gshi@xmu.edu.cn.
Yuan LiuDepartment of Rheumatology and Clinical Immunology, the First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, 55th, Zhenhai Road, Xiamen, XM, 361000, China. liuyuan@xmu.edu.cn.

Funding

National Natural Science Foundation of China 81971496National Natural Science Foundation of China 82171779Natural Science Foundation of Fujian Province 2023J06055Science Foundation of Fujian Province 2020J05309Science Foundation of Fujian Province 2021CXB021Science Foundation of Fujian Province 2021J05292Scientific and Technological Projects of Xiamen City 3502Z20209004
6 · The paper itself

Abstract

Fibroblast-like synoviocytes (FLSs) play a central role in RA pathogenesis and are the main cellular component in the inflamed synovium of patients with rheumatoid arthritis (RA). FLSs are emerging as promising new therapeutic targets in RA. However, fibroblasts perform many essential functions that are required for sustaining tissue homeostasis. Direct targeting of general fibroblast markers on FLSs is challenging because fibroblasts in other tissues might be altered and side effects such as reduced wound healing or fibrosis can occur. To date, no FLS-specific targeted therapies have been applied in the clinical management of RA. With the help of high-throughput technologies such as scRNA-seq in recent years, several specific pathogenic FLS subsets in RA have been identified. Understanding the characteristics of these pathogenic FLS clusters and the mechanisms that drive their differentiation can provide new insights into the development of novel FLS-targeting strategies for RA. Here, we discuss the pathogenic FLS subsets in RA that have been elucidated in recent years and potential strategies for targeting pathogenic FLSs.

Indexed as

Arthritis, RheumatoidFibroblastsSynoviocytesAnimalsCell DifferentiationHumansSynovial MembraneFibroblast-like synoviocytesImmune homeostasisInflammationRheumatoid arthritisTherapeutic target

Identifiers

PMID38783357
PMCPMC11112866

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.