Evidence map›Paper›PMID 36810113›Full record

ArticleJournal of inflammation (London, England)2023

Transient receptor potential melastatin 2 regulates neutrophil extracellular traps formation and delays resolution of neutrophil-driven sterile inflammation.

Xue Cao, Yanhong Li, Yubin Luo, Tianshu Chu, Hang Yang, Ji Wen, Yi Liu, Yi Zhao, Martin Herrmann

Open access · goldAbstract read
In one paragraph

Article in Journal of inflammation (London, England), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

12 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
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  12. Neutrophil extracellular traps in homeostasis and disease.Signal transduction and targeted therapy · 2024
    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

9 authors at 5 institutions in 2 countries.

Xue Cao *Department of Rheumatology and Immunology, West China Hospital, Sichuan University, Chengdu, Sichuan, China.
Yanhong Li *Department of Rheumatology and Immunology, West China Hospital, Sichuan University, Chengdu, Sichuan, China.
Yubin LuoDepartment of Rheumatology and Immunology, West China Hospital, Sichuan University, Chengdu, Sichuan, China.
Tianshu ChuDepartment of Rheumatology and Immunology, Henan Provincial People's Hospital, People's Hospital of Zhengzhou University, People's Hospital of Henan University, Zhengzhou, Henan, China.
Hang YangDepartment of Rheumatology and Immunology, West China Hospital, Sichuan University, Chengdu, Sichuan, China.
Ji WenDepartment of Rheumatology and Immunology, West China Hospital, Sichuan University, Chengdu, Sichuan, China.
Yi LiuDepartment of Rheumatology and Immunology, West China Hospital, Sichuan University, Chengdu, Sichuan, China.
Yi ZhaoDepartment of Rheumatology and Immunology, West China Hospital, Sichuan University, Chengdu, Sichuan, China. zhao.y1977@163.com.
Martin HerrmannDepartment of Internal Medicine 3, Rheumatology and Immunology, Friedrich-Alexander- University Erlangen-Nürnberg (FAU), Erlangen, Germany.
Sichuan University · CNWest China Hospital of Sichuan University · CNFriedrich-Alexander-Universität Erlangen-Nürnberg · DEHenan Provincial People's Hospital · CNZhengzhou University · CN

Funding

1·3·5 project for Outstanding interdisciplinary project of West China Hospital, Sichuan University ZYGD18015, ZYJC18003, ZYJC18024from zero to one Innovative Research Program of Sichuan University 2022SCUH0020National Key Research and Development Program of China 2019YFE0108200National Natural Science Foundation of China 82001728,81973540Sichuan International Science and Technology Innovation Cooperation/Hong Kong, Macao and Taiwan Science and Technology Innovation Cooperation Project 2022YFH0023the German Research Foundation projects DFG-SFB/TRR241 (B04) and DFG-SFB/CRC1181 (C03) DFG-SFB/TRR241 (B04),DFG-SFB/CRC1181 (C03)
6 · The paper itself

Abstract

The formation of neutrophil extracellular traps (NETs) is a process releasing into the extracellular space networks of chromatin fibers decorated with granular proteins. It is implicated in infection-related as well as sterile inflammation. Monosodium urate (MSU) crystals serve as damage-associated molecular pattern (DAMP) in various conditions of disease. Formation of NETs or aggregated NETs (aggNETs) orchestrates initiation and resolution of MSU crystals-triggered inflammation, respectively. Elevated intracellular calcium levels and the generation of reactive oxygen species (ROS) are crucial for the formation of MSU crystal-induced NETs. However, the exact signaling pathways involved are still elusive. Herein, we demonstrate that the ROS-sensing, non-selective calcium-permeable channel transient receptor potential cation channel subfamily M member 2 (TRPM2) is required for a full-blown MSU crystal-induced NET formation. Primary neutrophils from TRPM2

Indexed as

MSU crystalsNET formationNeutrophil extracellular trapsROSSterile inflammationTRPM2

Identifiers

PMID36810113
PMCPMC9945693
OpenAlexW4321611212

What OpenQuestion holds

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LicenceCC BY
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.