Evidence map›Paper›PMID 28827659›Full record

ArticleScientific reports2017

TDAG8, TRPV1, and ASIC3 involved in establishing hyperalgesic priming in experimental rheumatoid arthritis.

Wei-Shan Hsieh, Chia-Chi Kung, Shir-Ly Huang, Shih-Chang Lin, Wei-Hsin Sun

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
4.4field-weighted citation impact, top 5% 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

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Acid-sensing ion channels and their role in controlling pain in the post-operative stage.International journal of physiology, pathophysiology and pharmacology · 2026
    Review
  5. Article
  6. Pain mechanism and management strategy of rheumatoid arthritis.Frontiers in pain research (Lausanne, Switzerland) · 2025
    Review
  7. Activation of the proton-sensing GPCR, GPR65 on fibroblast-like synoviocytes contributes to inflammatory joint pain.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  8. Article
  9. Article
  10. Article
  11. Roles of TRP and PIEZO receptors in autoimmune diseases.Expert reviews in molecular medicine · 2024
    Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Review
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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

5 authors at 3 institutions in 1 country.

Wei-Shan HsiehDepartment of Life Sciences, National Central University, Zhongli, Taoyuan city, Taiwan.
Chia-Chi KungDepartment of Life Sciences, National Central University, Zhongli, Taoyuan city, Taiwan.
Shir-Ly HuangInstitute of Microbiology and Immunology, National Yang-Ming University, Taipei, Taiwan.
Shih-Chang LinDepartment of Immunology, Cathy General Hospital, Taipei, Taiwan.
Wei-Hsin SunDepartment of Life Sciences, National Central University, Zhongli, Taoyuan city, Taiwan. weihsin@cc.ncu.edu.tw.ORCID 0000-0003-3009-520X
National Central University · TWCathay General Hospital · TWNational Yang Ming Chiao Tung University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rheumatoid arthritis (RA), characterized by chronic inflammation of synovial joints, is often associated with ongoing pain and increased pain sensitivity. High hydrogen ion concentration (acidosis) found in synovial fluid in RA patients is associated with disease severity. Acidosis signaling acting on proton-sensing receptors may contribute to inflammation and pain. Previous studies focused on the early phase of arthritis (<5 weeks) and used different arthritis models, so elucidating the roles of different proton-sensing receptors in the chronic phase of arthritis is difficult. We intra-articularly injected complete Freund's adjuvant into mice once a week for 4 weeks to establish chronic RA pain. Mice with knockout of acid-sensing ion channel 3 (ASIC3) or transient receptor potential/vanilloid receptor subtype 1 (TRPV1) showed attenuated chronic phase (>6 weeks) of RA pain. Mice with T-cell death-associated gene 8 (TDAG8) knockout showed attenuated acute and chronic phases of RA pain. TDAG8 likely participates in the initiation of RA pain, but all three genes, TDAG8, TRPV1, and ASIC3, are essential to establish hyperalgesic priming to regulate the chronic phase of RA pain.

Indexed as

Acid Sensing Ion ChannelsAnimalsAntigens, CDAntigens, Differentiation, MyelomonocyticArthralgiaArthritis, ExperimentalArthritis, RheumatoidBiomarkersCD68 MoleculeCytokinesDisease Models, AnimalFemaleGene ExpressionHyperalgesiaImmunohistochemistryMacrophagesAcid Sensing Ion ChannelsAntigens, CDAntigens, Differentiation, MyelomonocyticASIC3 protein, mouseBiomarkersCD68 antigen, humanCD68 MoleculeCytokinesGPR65 protein, mouseReceptors, G-Protein-CoupledTRPV1 receptorTRPV Cation Channels

Identifiers

PMID28827659
PMCPMC5566336
OpenAlexW2749704992

What OpenQuestion holds

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LicenceCC BY
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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 OpenQuestion graph.