Evidence map›Paper›PMID 38055119›Full record

ArticleInflammation2024

Upregulation of CD39 During Gout Attacks Promotes Spontaneous Remission of Acute Gouty Inflammation.

Chengyu Luo, Xingyue Liu, Yiming Liu, Huijun Shao, Jie Gao, Jinhui Tao

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2024. 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, top 73% 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

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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, 0 citations in OpenAlex.

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

6 authors at 2 institutions in 1 country.

Chengyu LuoDepartment of Rheumatology and Immunology, Division of Life Sciences and Medicine, The First Affiliated Hospital of University of Science and Technology of China (USTC), University of Science and Technology of China, Hefei, 230001, People's Republic of China.
Xingyue LiuDepartment of Rheumatology and Immunology, Division of Life Sciences and Medicine, The First Affiliated Hospital of University of Science and Technology of China (USTC), University of Science and Technology of China, Hefei, 230001, People's Republic of China.
Yiming LiuDepartment of Rheumatology and Immunology, Division of Life Sciences and Medicine, The First Affiliated Hospital of University of Science and Technology of China (USTC), University of Science and Technology of China, Hefei, 230001, People's Republic of China.
Huijun ShaoDepartment of Rheumatology and Immunology, The Affiliated Provincial Hospital of Anhui Medical University, Hefei, 230001, People's Republic of China.
Jie GaoDepartment of Rheumatology and Immunology, Division of Life Sciences and Medicine, The First Affiliated Hospital of University of Science and Technology of China (USTC), University of Science and Technology of China, Hefei, 230001, People's Republic of China.
Jinhui TaoDepartment of Rheumatology and Immunology, Division of Life Sciences and Medicine, The First Affiliated Hospital of University of Science and Technology of China (USTC), University of Science and Technology of China, Hefei, 230001, People's Republic of China. taojinhui@ustc.edu.cn.
University of Science and Technology of China · CNAnhui Medical University · CN

Funding

Fundamental Research Funds for the Central Universities YD9110002017
6 · The paper itself

Abstract

Gout is a self-limiting form of inflammatory arthropathy caused by the formation of urate crystals due to hyperuricemia. The resolution of gout involves the transition of proinflammatory M1-type macrophages to anti-inflammatory M2-type macrophages, as well as neutrophil-mediated extracellular trap (NET) formation. However, the underlying mechanisms of these changes are not clear. Studies have confirmed that high expression of CD39 on macrophages and neutrophils can trigger the polarization of macrophages from a proinflammatory state to an anti-inflammatory state. Recent studies have shown that the pathogenesis of gout involves extracellular ATP (eATP), and the synergistic effect of MSU and extracellular ATP can cause gout. CD39 is a kind of ATP hydrolysis enzyme that can degrade eATP, suggesting that CD39 may inhibit the aggravation of inflammation in gout and participate in the remission mechanism of gout. To confirm this hypothesis, using data mining and flow cytometry, we first found that CD39 expression was significantly upregulated on CD14 + monocytes and neutrophils in gout patients during the acute phase. Inhibition of CD39 by lentivirus or a CD39 inhibitor in acute gout models aggravated gouty arthritis and delayed gout remission. Apyrase, a functional analog of CD39, can significantly reduce the inflammatory response and promote gout remission in acute gout model mice. Our findings confirm that the upregulation of CD39 during gout flare-ups promotes spontaneous remission of acute gouty inflammation.

Indexed as

ApyraseGoutUp-RegulationAnimalsAntigens, CDArthritis, GoutyInflammationMacrophagesMaleNeutrophilsRatsRats, Sprague-DawleyRemission, SpontaneousAntigens, CDApyraseCD39 antigenENTPD1 protein, humanCD39eATPgoutIL-1βNLRP3

Identifiers

PMID38055119
OpenAlexW4389397336

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.