Evidence map›Paper›PMID 40248103›Full record

ArticleFrontiers in pharmacology2025

Exploring the mechanism of triptolide inhibiting the motility of fibroblast-like synoviocytes in rheumatoid arthritis via RhoA/Rho-associated kinase axis, based on network pharmacology, molecular docking and molecular dynamics simulations.

Jiacheng Shen, Yuxuan Fang, Nan Xu, Hongyi Chen, Miao Zhu, Dan Li, Zewen Chu, Masataka Sunagawa, Yanqing Liu, Haibo Wang and 1 more

Abstract read
In one paragraph

Article in Frontiers in pharmacology, 2025. 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
–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

10 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Pharmaceuticals (Basel, Switzerland) · 2026
    Article
  7. Article
  8. Article
  9. Frontiers in immunology · 2026
    Review
  10. 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

11 authors.

Jiacheng Shen *Department of Rheumatology and Immunology, Affiliated Hospital of Yangzhou University, Yangzhou University, Yangzhou, Jiangsu, China.
Yuxuan Fang *Department of Rheumatology and Immunology, Affiliated Hospital of Yangzhou University, Yangzhou University, Yangzhou, Jiangsu, China.
Nan Xu *Department of Rheumatology and Immunology, Affiliated Hospital of Yangzhou University, Yangzhou University, Yangzhou, Jiangsu, China.
Hongyi ChenDepartment of Rheumatology and Immunology, Affiliated Hospital of Yangzhou University, Yangzhou University, Yangzhou, Jiangsu, China.
Miao ZhuMedical College, Institute of Translational Medicine, Yangzhou University, Yangzhou, China.
Dan LiMedical College, Institute of Translational Medicine, Yangzhou University, Yangzhou, China.
Zewen ChuSchool of Rehabilitation Science, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Masataka SunagawaDepartment of Physiology, School of Medicine, Showa University, Tokyo, Japan.
Yanqing LiuMedical College, Institute of Translational Medicine, Yangzhou University, Yangzhou, China.
Haibo WangMedical College, Institute of Translational Medicine, Yangzhou University, Yangzhou, China.
Guoqing LiDepartment of Rheumatology and Immunology, Affiliated Hospital of Yangzhou University, Yangzhou University, Yangzhou, Jiangsu, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background and objective: Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by the hyperproliferation and invasive behavior of rheumatoid arthritis fibroblast-like synoviocytes (RA-FLS), which contributes to the degradation of articular cartilage and bone. Inhibition of RA-FLS proliferation, migration and invasion has become an important therapeutic strategy for RA. Triptolide (TPL), an epoxy diterpene lactone compound from the traditional Chinese medicine Materials and methods: Results: TPL significantly inhibited RA-FLS cell motility, and reduced the displacement and cumulative distance of RA-FLS. Cytoskeleton staining assay and TEM observation showed cytoskeleton remodeling after TPL treatment. Network pharmacological prediction screened 45 targets associated with TPL intervention in RA via cytoskeleton, including TNF, KRAS, ESR1, RHOA, MAPK3 and CASP3. In the RhoA/Rho-associated kinase signaling pathway, TPL treatment inhibited protein expression and phosphorylation of RhoA, Rock, and Limk. TPL can enter RhoA, Rock1, and Rock2 target protein binding domains with stable binding activities, and may cause conformational changes of Rock1 related to molecular functions. Conclusion: TPL inhibits RA-FLS in motility by regulating actin cytoskeleton remodeling through action on the RhoA/Rho-associated kinase signaling pathway.

Indexed as

cytoskeletonmolecular dynamics simulationsnetwork pharmacologyrheumatoid arthritisRhoA/Rho-associated kinasetriptolide

Identifiers

PMID40248103
PMCPMC12003270

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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.