ArticleArthritis research & therapy2025
KLF11 alleviates rheumatoid arthritis by regulating M1 macrophage polarization via downregulation of YAP1 expression.
Article in Arthritis research & therapy, 2025. 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.
- Bmal1 Attenuates Collagen-Induced Arthritis by Regulating Macrophage Polarization via Sirt1.Journal of inflammation research · 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
6 authors.
Funding
Abstract
Rheumatoid arthritis (RA) is a chronic autoimmune disease, primarily impacting joints and bones. The Gene Expression Omnibus (GEO) datasets (GSE55235 and GSE10500) revealed that KLF11 expression was lower in the patients with RA, which was confirmed by the collected RA samples. However, KLF11's function and molecular mechanism in RA remain to be elucidated. In our study, we investigated this issue using in vivo and in vitro models. Our findings consistently demonstrated the downregulation of KLF11 in mice with collagen-induced arthritis (CIA). Overexpression of KLF11 reduced the arthritis severity and the extent of bone destruction in mice with CIA, whereas KLF11 knockdown exerted the opposite effect. Additionally, it was noted to inhibit M1 macrophage polarization and the ERK pathway both in vivo and in vitro. The JASPAR database indicated the potential for KLF11 to bind to the YAP1 promoter region. ChIP and dual-luciferase reporter assays confirmed the binding of KLF11 to the promoter of YAP1. Further experiments demonstrated that KLF11 negatively regulated YAP1 expression in THP-1 cells. YAP1 overexpression partially reversed the KLF11's inhibitory effect on the ERK signaling pathway and M1 macrophage polarization in vitro. KLF11 may be a promising 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.