Evidence map›Paper›PMID 38796413›Full record

ArticleJournal of translational medicine2024

Atox1 regulates macrophage polarization in intestinal inflammation via ROS-NLRP3 inflammasome pathway.

MingXian Chen, Yu Chen, Rui Fu, SaiYue Liu, HaiXia Li, TangBiao Shen

Abstract read
In one paragraph

Article in Journal of translational medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing 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

17 citing papers in PubMed.

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  6. The AGO2-ATOX1 axis exacerbates inflammation in a mouse sepsis model.Central-European journal of immunology · 2026
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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

6 authors.

MingXian ChenDepartment of Gastroenterology, Tongde Hospital of Zhejiang Province, No. 234, Gucui road, Hangzhou, 310012, China.
Yu ChenLaboratory Animal Center, Zhejiang Province Academy of Traditional Chinese Medicine, Hangzhou, 310012, China.
Rui FuDepartment of Gastroenterology, Tongde Hospital of Zhejiang Province, No. 234, Gucui road, Hangzhou, 310012, China.
SaiYue LiuDepartment of Adverse Drug Reaction Monitoring, Zhejiang Province Center of Adverse Drug Reaction Monitoring, No. 39, Yile road, Hangzhou, 310012, China. liusaiyue@163.com.
HaiXia LiDepartment of Cardiology, Guanganmen Hospital of China Academy of Chinese Medical Sciences, No. 5, Beixian Ge, Xicheng District, Beijing, 100053, China. 2272236055@qq.com.
TangBiao ShenDepartment of Gastroenterology, Tongde Hospital of Zhejiang Province, No. 234, Gucui road, Hangzhou, 310012, China. shentangbiao@126.com.

Funding

State Administration of Traditional Chinese Medicine Science and Technology Department-Zhejiang Provincial Administration of Traditional Chinese Medicine Co-construction of Key laboratory GZY-ZJ-SY-2402Zhejiang Province 551 Health Talent Training Project Zhejiang Provincial Health and Health Commission Office [2021] 40Zhejiang Provincial Natural Science Foundation of China LY21H270003
6 · The paper itself

Abstract

backgroundInflammation and oxidative stress play an important role in the pathophysiology of inflammatory bowel disease (IBD). This study aimed to explore the effects of copper chaperone Antioxidant-1 (Atox1) on macrophages in a mouse model of intestinal inflammation.

methodsA mouse model of TNBS-induced colitis was established and verified using the disease activity index. Atox1 conditional knockout mice were applied. The proportion of macrophages in colonic lamina propria mononuclear cells and ROS production were analyzed using flow cytometry. Inflammatory cytokines were measured using ELISA. Expression of macrophage M1/M2 polarization markers, p47phox, NLRP3, and Caspase-1 p20 was measured using quantitative RT-PCR and Western blotting.

resultsAtox1 expression was up-regulated in colon tissues of TNBS-induced colitis mice. Macrophages isolated from TNBS-induced colitis mice showed M1 polarization and nuclear translocation of Atox1. Inhibiting copper chaperone activity decreased p47phox, ROS production, and M1 polarization induced by CuCl

conclusionAtox1 plays a pro-inflammatory role, promotes M1 polarization of macrophages, and increases the concentrations of pro-inflammatory cytokines in intestinal tissue by regulating the ROS-NLRP3 inflammasome pathway. Atox1 is a potential therapeutic target in IBD.

Indexed as

Cell PolarityColitisInflammasomesInflammationMacrophagesMice, KnockoutNLR Family, Pyrin Domain-Containing 3 ProteinReactive Oxygen SpeciesSignal TransductionAnimalsCytokinesIntestinesMaleMiceMice, Inbred C57BLMolecular ChaperonesCytokinesInflammasomesMolecular ChaperonesNLR Family, Pyrin Domain-Containing 3 ProteinReactive Oxygen SpeciesTrinitrobenzenesulfonic AcidCopper metabolismInflammatory bowel diseaseMacrophage polarizationNLRP3 inflammasomeROS

Identifiers

PMID38796413
PMCPMC11128112

What Socratic 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 Socratic graph.