Evidence map›Paper›PMID 41790423›Full record

ArticleNeuroscience bulletin2026

Tissue-Resident Macrophage PIEZO1 Transduces Mechanical Stress into Inflammatory Pain in Acute Gout.

Tianyi Shen, Ting Wang, Liyan Wu, Zihan Wang, Liqin Gan, Yubin Luo, Cong Liu, Yang Xu, De-An Guo, Qirui Bi and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neuroscience bulletin, 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

14 authors.

Tianyi Shen *State Key Laboratory of Chemical Biology, Shanghai Institute of Materia Medica, Chinese Academy of Science, Shanghai, 201203, China.ORCID http://orcid.org/0009-0008-9942-6971
Ting Wang *State Key Laboratory of Chemical Biology, Shanghai Institute of Materia Medica, Chinese Academy of Science, Shanghai, 201203, China.ORCID http://orcid.org/0000-0003-4717-9530
Liyan WuState Key Laboratory of Chemical Biology, Shanghai Institute of Materia Medica, Chinese Academy of Science, Shanghai, 201203, China.ORCID http://orcid.org/0009-0003-1169-5426
Zihan WangState Key Laboratory of Chemical Biology, Shanghai Institute of Materia Medica, Chinese Academy of Science, Shanghai, 201203, China.
Liqin GanShanghai Research Center for Modernization of Traditional Chinese Medicine, National Engineering Laboratory for TCM Standardization Technology, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China.
Yubin LuoDepartment of Rheumatology and Immunology, Laboratory of Rheumatology and Immunology, Frontiers Science Center for Disease-related Molecular Network, West China Hospital, Sichuan University, Chengdu, 610064, China.
Cong LiuInternational Cooperation Base for Active Substances in Traditional Chinese Medicine in Hubei Province, School of Pharmaceutical Sciences, South-Central Minzu University, Wuhan, 430074, China.
Yang XuDepartment of Orthopedics, West China Hospital, Sichuan University, Chengdu, 610041, China.
De-An GuoUniversity of Chinese Academy of Sciences, Beijing, 100049, China.
Qirui BiShanghai Research Center for Modernization of Traditional Chinese Medicine, National Engineering Laboratory for TCM Standardization Technology, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China.
Wanying WuUniversity of Chinese Academy of Sciences, Beijing, 100049, China.
Lvyi ChenSchool of Pharmaceutical Sciences, South-Central Minzu University, Wuhan, 430074, China.
Yi ChangYangpu Hospital, School of Medicine, Tongji University, Shanghai, 200092, China. chani_1213@163.com.
Jing FengState Key Laboratory of Chemical Biology, Shanghai Institute of Materia Medica, Chinese Academy of Science, Shanghai, 201203, China. fengjing@simm.ac.cn.ORCID http://orcid.org/0000-0001-6726-7912

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gouty arthritis is an autoinflammatory joint disease caused by the deposition of monosodium urate crystals, which activate innate immune responses and elicit acute episodes of joint pain and inflammation. Although macrophages are key players in recognizing monosodium urate (MSU) crystals and initiating the inflammatory cascade, the specific contribution of tissue-resident macrophages and their mechanosensory machinery remains unclear. Here, we identify the mechanosensitive ion channel PIEZO1 as a critical mediator of inflammation and pain in MSU-induced acute gout. We show that synovial CX3CR1

Indexed as

Arthritis, GoutyGoutInflammationIon ChannelsMacrophagesMechanotransduction, CellularPainAnimalsCX3C Chemokine Receptor 1Disease Models, AnimalHumansMaleMiceMice, Inbred C57BLStress, MechanicalUric AcidCX3C Chemokine Receptor 1Ion ChannelsPiezo1 protein, mouseUric AcidGouty arthritisIL-1βPIEZO1Tissue-resident macrophage

Identifiers

PMID41790423
PMCPMC13388588

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.