Evidence map›Paper›PMID 35464445›Full record

ReviewFrontiers in immunology2022

Inflammatory Response to Regulated Cell Death in Gout and Its Functional Implications.

Jianan Zhao, Kai Wei, Ping Jiang, Cen Chang, Lingxia Xu, Linshuai Xu, Yiming Shi, Shicheng Guo, Yu Xue, Dongyi He

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed, 3 pooled it
12.2field-weighted citation impact, top 1% 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

61 citing papers in PubMed, 3 syntheses or guidelines pooled it, 91 citations in OpenAlex.

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  14. Standardized Extract of Flavonoids fromJournal of inflammation research · 2026
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1 more citing papers are in PubMed but not listed here.

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

10 authors at 4 institutions in 2 countries.

Jianan ZhaoGuanghua Clinical Medical College, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Kai WeiGuanghua Clinical Medical College, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Ping JiangGuanghua Clinical Medical College, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Cen ChangGuanghua Clinical Medical College, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Lingxia XuGuanghua Clinical Medical College, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Linshuai XuGuanghua Clinical Medical College, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Yiming ShiGuanghua Clinical Medical College, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Shicheng GuoComputation and Informatics in Biology and Medicine, University of Wisconsin-Madison, Madison, WI, United States.
Yu XueDepartment of Rheumatology, Huashan Hospital, Institute of Rheumatology, Immunology and Allergy, Fudan University, Shanghai, China.
Dongyi HeGuanghua Clinical Medical College, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Shanghai Guanghua Hospital of Integrated Traditional Chinese and Western Medicine · CNShanghai University of Traditional Chinese Medicine · CNFudan University · CNUniversity of Wisconsin–Madison · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gout, a chronic inflammatory arthritis disease, is characterized by hyperuricemia and caused by interactions between genetic, epigenetic, and metabolic factors. Acute gout symptoms are triggered by the inflammatory response to monosodium urate crystals, which is mediated by the innate immune system and immune cells (e.g., macrophages and neutrophils), the NACHT, LRR, and PYD domains-containing protein 3 (NLRP3) inflammasome activation, and pro-inflammatory cytokine (e.g., IL-1β) release. Recent studies have indicated that the multiple programmed cell death pathways involved in the inflammatory response include pyroptosis, NETosis, necroptosis, and apoptosis, which initiate inflammatory reactions. In this review, we explore the correlation and interactions among these factors and their roles in the pathogenesis of gout to provide future research directions and possibilities for identifying potential novel therapeutic targets and enhancing our understanding of gout pathogenesis.

Indexed as

Arthritis, GoutyGoutHumansInflammasomesMacrophagesPyroptosisInflammasomesapoptosisgoutinflammationnecroptosisNETosisprogrammed cell deathpyroptosis

Identifiers

PMID35464445
PMCPMC9020265
OpenAlexW4225469642

What OpenQuestion holds

Textmetadata
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.