Evidence map›Paper›PMID 40125663›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025

Eosinophils-Induced Lumican Secretion by Synovial Fibroblasts Alleviates Cartilage Degradation via the TGF-β Pathway Mediated by Anxa1 Binding.

Wenqian Chen, Yuwei Zhou, Wenxiu Yuan, Yanjing Ou, Hanyu Lin, Kaixun He, Xueshen Qian, Huachen Chen, Chengchaozi Wang, Jie Lu and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Review
  3. 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

13 authors.

Wenqian ChenFujian Key Laboratory of Oral Diseases & Fujian Provincial Engineering Research Center of Oral Biomaterial & Stomatological Key Lab of Fujian College and University, School and Hospital of Stomatology, Fujian Medical University, Fuzhou, Fujian, 350002, P. R. China.
Yuwei ZhouFujian Key Laboratory of Oral Diseases & Fujian Provincial Engineering Research Center of Oral Biomaterial & Stomatological Key Lab of Fujian College and University, School and Hospital of Stomatology, Fujian Medical University, Fuzhou, Fujian, 350002, P. R. China.
Wenxiu YuanFujian Key Laboratory of Oral Diseases & Fujian Provincial Engineering Research Center of Oral Biomaterial & Stomatological Key Lab of Fujian College and University, School and Hospital of Stomatology, Fujian Medical University, Fuzhou, Fujian, 350002, P. R. China.
Yanjing OuFujian Key Laboratory of Oral Diseases & Fujian Provincial Engineering Research Center of Oral Biomaterial & Stomatological Key Lab of Fujian College and University, School and Hospital of Stomatology, Fujian Medical University, Fuzhou, Fujian, 350002, P. R. China.
Hanyu LinFujian Key Laboratory of Oral Diseases & Fujian Provincial Engineering Research Center of Oral Biomaterial & Stomatological Key Lab of Fujian College and University, School and Hospital of Stomatology, Fujian Medical University, Fuzhou, Fujian, 350002, P. R. China.
Kaixun HeFujian Key Laboratory of Oral Diseases & Fujian Provincial Engineering Research Center of Oral Biomaterial & Stomatological Key Lab of Fujian College and University, School and Hospital of Stomatology, Fujian Medical University, Fuzhou, Fujian, 350002, P. R. China.
Xueshen QianFujian Key Laboratory of Oral Diseases & Fujian Provincial Engineering Research Center of Oral Biomaterial & Stomatological Key Lab of Fujian College and University, School and Hospital of Stomatology, Fujian Medical University, Fuzhou, Fujian, 350002, P. R. China.
Huachen ChenFujian Key Laboratory of Oral Diseases & Fujian Provincial Engineering Research Center of Oral Biomaterial & Stomatological Key Lab of Fujian College and University, School and Hospital of Stomatology, Fujian Medical University, Fuzhou, Fujian, 350002, P. R. China.
Chengchaozi WangFujian Key Laboratory of Oral Diseases & Fujian Provincial Engineering Research Center of Oral Biomaterial & Stomatological Key Lab of Fujian College and University, School and Hospital of Stomatology, Fujian Medical University, Fuzhou, Fujian, 350002, P. R. China.
Jie LuFujian Key Laboratory of Oral Diseases & Fujian Provincial Engineering Research Center of Oral Biomaterial & Stomatological Key Lab of Fujian College and University, School and Hospital of Stomatology, Fujian Medical University, Fuzhou, Fujian, 350002, P. R. China.
Weiping ChenFujian Key Laboratory of Oral Diseases & Fujian Provincial Engineering Research Center of Oral Biomaterial & Stomatological Key Lab of Fujian College and University, School and Hospital of Stomatology, Fujian Medical University, Fuzhou, Fujian, 350002, P. R. China.
Dexiong LiFujian Key Laboratory of Oral Diseases & Fujian Provincial Engineering Research Center of Oral Biomaterial & Stomatological Key Lab of Fujian College and University, School and Hospital of Stomatology, Fujian Medical University, Fuzhou, Fujian, 350002, P. R. China.
Jiang ChenFujian Key Laboratory of Oral Diseases & Fujian Provincial Engineering Research Center of Oral Biomaterial & Stomatological Key Lab of Fujian College and University, School and Hospital of Stomatology, Fujian Medical University, Fuzhou, Fujian, 350002, P. R. China.ORCID https://orcid.org/0000-0001-6879-6525

Funding

National Natural Science Foundation of China 81771126National Natural Science Foundation of China 82371008Natural Science Foundation, Fujian Province 2023J01703Natural Science Foundation, Fujian Province 2024J01649Startup Fund for Scientific Research, Fujian Medical University 2023QH1146Startup Fund for Scientific Research, Fujian Medical University 2023QH2016
6 · The paper itself

Abstract

The innate immune response is crucial in the progression of temporomandibular joint osteoarthritis (TMJOA). Yet, the roles of eosinophils in TMJOA remain unclear, underscoring the need for further investigation into their potential impact and mechanism. Addressing the clinical observation that eosinophil numbers in synovial fluid are higher in healthy individuals than in those with TMJOA, the vital regulation of this cell population in TMJOA by using an ovalbumin (OVA)-induced hyper-eosinophilia asthma rats is explored and a rat model of antibody-mediated eosinophil depletion in vivo, and co-culture system of synovial fibroblasts, chondrocytes, and eosinophils in vitro. The abnormal synovial proliferation, cartilage degradation, and subchondral bone erosion are effectively inhibited in OVA-induced asthmatic rats appearing in the local accumulation of eosinophils in the synovium. Conversely, the reduction in synovial eosinophils exacerbated TMJOA in rats treated with TRFK. Mechanistically, the protective effect of eosinophils against TMJOA is attributed to their promotion of Lumican secretion in the synovium, where Lumican binds to Annexin A1 in chondrocytes, inhibits transforming growth factor β2 Annexin A1 and Smad2/3 phosphorylation. These results illustrate OVA/IL-5-induced eosinophils' crucial role in TMJOA, identifying Lumican as a key anti-TMJOA target. Collectively, these findings revealed the signature and mechanism in eosinophils that stimulate TMJOA resolution.

Indexed as

Annexin A1EosinophilsFibroblastsOsteoarthritisSynovial MembraneTransforming Growth Factor betaAnimalsChondrocytesDisease Models, AnimalMaleRatsRats, Sprague-DawleySignal TransductionAnnexin A1Transforming Growth Factor betaAnxa1cartilageeosinophilsLumicantemporomandibular joint osteoarthritisTGFβ2

Identifiers

PMID40125663
PMCPMC12362735

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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.