ArticleMediators of inflammation2026
NR1D1-Mediated Suppression of JAK1/STAT3 Signaling Contributes to the Therapeutic Effects of Triptolide in Rheumatoid Arthritis.
Article in Mediators of inflammation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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.
Who cites it
1 citing paper in PubMed.
- NR1D1-Mediated Suppression of JAK1/STAT3 Signaling Contributes to the Therapeutic Effects of Triptolide in Rheumatoid Arthritis.Mediators of inflammation · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
backgroundTriptolide demonstrates potent antiarthritic effects in rheumatoid arthritis (RA), although its complete mechanism is not fully elucidated. This study aimed to systematically identify its core targets and regulatory pathways by integrating network pharmacology, molecular docking, and experimental validation.
methodsPotential targets of triptolide and RA-associated genes were sourced from public databases. Network module analysis identified key targets, the binding affinity of which to triptolide was subsequently assessed by molecular docking, molecular dynamics (MD) simulations, and drug affinity responsive target stability (DARTS) assay. The functional effects of triptolide on RA fibroblast-like synoviocytes (RA-FLS) behavior, joint inflammation, and bone erosion were further investigated using in vitro cellular assays and a collagen-induced arthritis (CIA) mouse model.
resultsOur analysis identified 73 candidate targets for triptolide against RA, which were primarily enriched in biological processes such as transcription factor activity and inflammatory response. Protein-protein interaction (PPI) network analysis highlighted a core module of five genes, among which STAT3 and its upstream regulator NR1D1 were selected for subsequent investigation. Molecular docking, MD simulation, and DARTS assay confirmed the high-affinity and direct binding of triptolide to NR1D1. In vitro, triptolide effectively suppressed RA-FLS migration and invasion, upregulated NR1D1, and inhibited JAK1/STAT3 signaling. In vivo, triptolide administration ameliorated arthritis severity and reduced bone erosion in CIA mice, as well as modulation of the NR1D1/STAT3 axis.
conclusionThis study demonstrates that triptolide alleviates RA through NR1D1-mediated inhibition of JAK1/STAT3 signaling. Our findings elucidate a novel molecular mechanism for triptolide's antiarthritic effects, thereby revealing the NR1D1/JAK1/STAT3 axis as a potential therapeutic target for RA.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.