Evidence map›Paper›PMID 41909682›Full record

ArticleFrontiers in immunology2026

Wilforine attenuates inflammatory osteolysis by suppressing osteoclast fusion through JAK-STAT-stomatin immunoregulatory signaling.

Shaohui Geng, Yiwei Guan, Zi Ye, Dongdong Zhao, Yijin Jiang, Jingyuan Fu, Han Sheng, Shuhan Yang, Hongxu Liu, Fuwen Deng and 5 more

Abstract read
In one paragraph

Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

15 authors.

Shaohui Geng *School of Life Science, Beijing University of Chinese Medicine, Beijing, China.
Yiwei Guan *School of Chinese Materia Medica, Beijing University of Chinese Medicine, Beijing, China.
Zi Ye *School of Chinese Materia Medica, Beijing University of Chinese Medicine, Beijing, China.
Dongdong Zhao *School of Life Science, Beijing University of Chinese Medicine, Beijing, China.
Yijin JiangSchool of Chinese Materia Medica, Beijing University of Chinese Medicine, Beijing, China.
Jingyuan FuSchool of Chinese Materia Medica, Beijing University of Chinese Medicine, Beijing, China.
Han ShengDongzhimen Hospital, Beijing University of Chinese Medicine, Beijing, China.
Shuhan YangSchool of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing, China.
Hongxu LiuSchool of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing, China.
Fuwen DengSchool of Nursing, Beijing University of Chinese Medicine, Beijing, China.
Shasha YuSchool of Life Science, Beijing University of Chinese Medicine, Beijing, China.
Mureziya YimingjiangSchool of Life Science, Beijing University of Chinese Medicine, Beijing, China.
Yuanhao WuFirst Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin, China.
Chen LiShanghai GuangHua Hospital of Integrated Traditional Chinese and Western Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Guangrui HuangSchool of Life Science, Beijing University of Chinese Medicine, Beijing, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Excessive osteoclast fusion and activation are central drivers of bone erosion in inflammatory osteopathies, which are closely linked to immune dysregulation. Wilforine, a natural compound, exhibits immunomodulatory and therapeutic potential, yet its precise mechanism of action-particularly its influence on the osteoclast membrane microenvironment and associated immune signaling-remains incompletely understood. Methods: We employed a multi-level strategy combining Results: Wilforine significantly alleviated bone erosion, marrow edema, and inflammatory infiltration Conclusion: This study defines a novel immunometabolic mechanism wherein Wilforine inhibits osteoclast fusion and bone resorption by reprogramming cellular lipid metabolism and disrupting the "JAK-STAT - Stomatin - Lipid Raft" functional axis. It highlights lipid rafts as a viable immunomodulatory microenvironment in bone disorders and provides a strong multi-omics-supported rationale for developing Wilforine as a bone-targeted immunotherapeutic agent.

Indexed as

Janus KinasesOsteoclastsOsteolysisSignal TransductionAnimalsDisease Models, AnimalInflammationMembrane ProteinsMiceJanus KinasesMembrane Proteinsbone erosionimmunometabolismlipid raftsosteoclast fusionSAPHO syndromestomatinwilforine

Identifiers

PMID41909682
PMCPMC13021455

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.