Evidence map›Paper›PMID 35292659›Full record

ArticleCell death & disease2022

Dopamine D3 receptor signaling alleviates mouse rheumatoid arthritis by promoting Toll-like receptor 4 degradation in mast cells.

Biao Wang, Xueyi Li, Ming Li, Yan Geng, Na Wang, Yaofeng Jin, Wen Zhang, Ke Xu, Jing Wang, Li Tao and 8 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.3field-weighted citation impact, top 21% of its field
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

11 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Dopamine D2 receptor on CD4Arthritis research & therapy · 2023
    Article
  10. Article
  11. Review
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

18 authors at 5 institutions in 1 country.

Biao WangDepartment of Immunology and Pathogenic Biology, College of Basic Medicine, Xi'an Jiaotong University Health Science Center, Xi'an, 710061, People's Republic of China.
Xueyi LiDepartment of Rheumatology, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710004, People's Republic of China.
Ming LiDepartment of Cardiovascular Surgery, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710061, People's Republic of China.
Yan GengDepartment of Clinical Laboratory, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710004, People's Republic of China.
Na WangCore Research Laboratory, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710004, People's Republic of China.
Yaofeng JinDepartment of Pathology, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710004, People's Republic of China.
Wen ZhangDepartment of Pathology, Northwest Women's and Children's Hospital, Xi'an, 710061, People's Republic of China.
Ke XuDepartment of Joint Surgery, Xi'an Hong Hui Hospital, Xi' an Jiaotong University Health Science Center, Xi'an, 710049, People's Republic of China.
Jing WangDepartment of Rheumatology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710061, People's Republic of China.
Li TaoDepartment of Clinical Laboratory, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710004, People's Republic of China.
Simin LaiDepartment of Immunology and Pathogenic Biology, College of Basic Medicine, Xi'an Jiaotong University Health Science Center, Xi'an, 710061, People's Republic of China.
Kunyi WuCore Research Laboratory, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710004, People's Republic of China.
Jing LeiDepartment of Clinical Laboratory, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710004, People's Republic of China.
Jing WangDepartment of Immunology and Pathogenic Biology, College of Basic Medicine, Xi'an Jiaotong University Health Science Center, Xi'an, 710061, People's Republic of China.
Ting ZhouDepartment of Clinical Laboratory, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710004, People's Republic of China.
Ke LiCore Research Laboratory, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710004, People's Republic of China. ke.li@mail.xjtu.edu.cn.
Yanjiong ChenDepartment of Immunology and Pathogenic Biology, College of Basic Medicine, Xi'an Jiaotong University Health Science Center, Xi'an, 710061, People's Republic of China. chenyanjiong@mail.xjtu.edu.cn.
Li XueDepartment of Clinical Laboratory, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710004, People's Republic of China. xuelially@163.com.ORCID 0000-0001-8580-6609
Second Affiliated Hospital of Xi'an Jiaotong University · CNFirst Affiliated Hospital of Xi'an Jiaotong University · CNXi'an Jiaotong University · CNNorthwest Women's and Children's Hospital · CNXi'an Honghui Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dopamine receptors are involved in several immunological diseases. We previously found that dopamine D3 receptor (D3R) on mast cells showed a high correlation with disease activity in patients with rheumatoid arthritis, but the mechanism remains largely elusive. In this study, a murine collagen-induced arthritis (CIA) model was employed in both DBA/1 mice and D3R knockout mice. Here, we revealed that D3R-deficient mice developed more severe arthritis than wild-type mice. D3R suppressed mast cell activation in vivo and in vitro via a Toll-like receptor 4 (TLR4)-dependent pathway. Importantly, D3R promoted LC3 conversion to accelerate ubiquitin-labeled TLR4 degradation. Mechanistically, D3R inhibited mTOR and AKT phosphorylation while enhancing AMPK phosphorylation in activated mast cells, which was followed by autophagy-dependent protein degradation of TLR4. In total, we found that D3R on mast cells alleviated inflammation in mouse rheumatoid arthritis through the mTOR/AKT/AMPK-LC3-ubiquitin-TLR4 signaling axis. These findings identify a protective function of D3R against excessive inflammation in mast cells, expanding significant insight into the pathogenesis of rheumatoid arthritis and providing a possible target for future treatment.

Indexed as

Arthritis, RheumatoidReceptors, Dopamine D3AMP-Activated Protein KinasesAnimalsHumansInflammationMast CellsMiceMice, Inbred DBAMice, KnockoutProto-Oncogene Proteins c-aktToll-Like Receptor 4TOR Serine-Threonine KinasesUbiquitinAMP-Activated Protein KinasesProto-Oncogene Proteins c-aktReceptors, Dopamine D3Toll-Like Receptor 4TOR Serine-Threonine KinasesUbiquitin

Identifiers

PMID35292659
PMCPMC8924203
OpenAlexW4220990367

What OpenQuestion holds

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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.