Evidence map›Paper›PMID 41495584›Full record

ArticleInflammation2026

Bone Morphogenetic Protein 6 Attenuates Psoriasis Pathogenesis by Suppressing Th17 Cell Differentiation.

Jingfei Fu, Yingyi Chen, Rui Zhao, Bingqing Wu, Juan Du, Junji Xu, Yi Liu

Abstract read
In one paragraph

Article in Inflammation, 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

7 authors.

Jingfei FuLaboratory of Tissue Regeneration and Immunology, Department of Periodontics, Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction, School of Stomatology, Capital Medical University, Beijing, China.
Yingyi ChenLaboratory of Tissue Regeneration and Immunology, Department of Periodontics, Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction, School of Stomatology, Capital Medical University, Beijing, China.
Rui ZhaoLaboratory of Tissue Regeneration and Immunology, Department of Periodontics, Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction, School of Stomatology, Capital Medical University, Beijing, China.
Bingqing WuLaboratory of Tissue Regeneration and Immunology, Department of Periodontics, Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction, School of Stomatology, Capital Medical University, Beijing, China.
Juan DuLaboratory of Tissue Regeneration and Immunology, Department of Periodontics, Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction, School of Stomatology, Capital Medical University, Beijing, China.
Junji XuCollege of Stomatology, Chongqing Key Laboratory of Oral Diseases and Biomedical Sciences, Chongqing Municipal Key Laboratory of Oral Biomedical Engineering of Higher Education, Chongqing Medical University, Chongqing, China. uujkl@163.com.
Yi LiuLaboratory of Tissue Regeneration and Immunology, Department of Periodontics, Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction, School of Stomatology, Capital Medical University, Beijing, China. lililiuyi@163.com.

Funding

the Innovation Research Team Project of Beijing Stomatological Hospital, Capital Medical University CXTD202202the National Key R&D of Program of China 2022YFC2504200the National Nature Science Foundation of China 82122015the Young Scientist Program Of Beijing Stomatological Hospital, Capital Medical University YSP202402
6 · The paper itself

Abstract

Bone morphogenetic protein (BMP) signaling has multiple functions in immune cells, especially in the differentiation of T cells. Previously, we found that BMP6 can dramatically promote the IFN-γ production in Th1. However, the interactions between BMP6 and Th17 cells remain poorly characterized. The evidence implicates dysregulated Th17 cell differentiation as a pivotal mechanism in psoriatic pathogenesis, yet the therapeutic potential of BMP6 in this autoimmune disease needs to be further explored. This study aimed to evaluate the potentially beneficial role of BMP6 in the Th17-induced psoriatic models and investigate its possible mechanisms. Th17 cells were intervened with BMP6 in vitro. The differentiation of Th17 was observed through multi-platform assessment combining flow cytometry, qRT-PCR, and ELISA. Signaling pathway activation was evaluated by Western blotting. RNAseq was used to further discover the impact of BMP6 on Th17. For in vivo experiments, the psoriatic model of C57BL/6 mice was established and treated with BMP6 i.d., and the Th17 cells were evaluated by flow cytometry. BMP6 treatment suppressed Th17 differentiation via the Smad1/5/9 pathway and impaired mitochondrial metabolism of Th17. In the imiquimod-induced psoriatic murine model, pharmacological BMP6 administration significantly attenuated disease progression and downregulated pathogenic Th17 cell frequency in lesional skin. Our finding elucidates the potential mechanism underlying the inhibitory effects of BMP6 in Th17-induced autoimmune diseases and furnish a theoretical foundation for its clinical application.

Indexed as

Bone Morphogenetic Protein 6Cell DifferentiationPsoriasisTh17 CellsAnimalsMiceMice, Inbred C57BLSignal TransductionBone Morphogenetic Protein 6BMP6Mitochondrial metabolismPsoriasisTh17 cell

Identifiers

PMID41495584
PMCPMC12832584

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Registered trials

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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.