Evidence map›Paper›PMID 30774633›Full record

ArticleFrontiers in immunology2019

Deficiency in IL-33/ST2 Axis Reshapes Mitochondrial Metabolism in Lipopolysaccharide-Stimulated Macrophages.

Huadan Xu, Liankun Sun, Yichun He, Xiaofeng Yuan, Junqi Niu, Jing Su, Dong Li

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 14% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. ST2 Signaling Regulates Innate Immune Responses in Kidney Injury.bioRxiv : the preprint server for biology · 2026
    Article
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  13. Suppression ofFrontiers in microbiology · 2022
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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

7 authors at 3 institutions in 1 country.

Huadan XuKey Laboratory of Pathobiology, Ministry of Education, Department of Pathophysiology, College of Basic Medical Sciences, Jilin University, Changchun, China.
Liankun SunKey Laboratory of Pathobiology, Ministry of Education, Department of Pathophysiology, College of Basic Medical Sciences, Jilin University, Changchun, China.
Yichun HeDepartment of Neurosurgery, China-Japan Union Hospital, Jilin University, Changchun, China.
Xiaofeng YuanDepartment of Pediatrics, Affiliated Hospital of Changchun University of Chinese Medicine, Changchun, China.
Junqi NiuDepartment of Hepatology, The First Hospital of Jilin University, Changchun, China.
Jing SuKey Laboratory of Pathobiology, Ministry of Education, Department of Pathophysiology, College of Basic Medical Sciences, Jilin University, Changchun, China.
Dong LiDepartment of Hepatology, The First Hospital of Jilin University, Changchun, China.
Jilin University · CNChangchun University of Chinese Medicine · CNFirst Hospital of Jilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The polarization and function of macrophages play essential roles in controlling immune responses. Interleukin (IL)-33 is a member of the IL-1 family that has been shown to influence macrophage activation and polarization, but the underlying mechanisms are not fully understood. Mitochondrial metabolism has been reported to be a central player in shaping macrophage polarization; previous studies have shown that both aerobic glycolysis and oxidative phosphorylation uniquely regulate the functions of M1 and M2 macrophages. Whether IL-33 polarizes macrophages by reshaping mitochondrial metabolism requires further investigation. In this work, we examined the mitochondrial metabolism of bone marrow-derived macrophages (BMDMs) from either wild type (WT),

Indexed as

AnimalsCell DifferentiationCells, CulturedDNA, MitochondrialInterleukin-1 Receptor-Like 1 ProteinInterleukin-33LipopolysaccharidesMacrophagesMaleMiceMice, Inbred BALB CMice, KnockoutMitochondriaPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaSignal TransductionDNA, MitochondrialIl1rl1 protein, mouseInterleukin-1 Receptor-Like 1 ProteinInterleukin-33LipopolysaccharidesPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPpargc1a protein, mouseATPIL-33macrophagePGC1αST2

Identifiers

PMID30774633
PMCPMC6367255
OpenAlexW2914146940

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.