Evidence map›Paper›PMID 33628592›Full record

ArticleCancer biology & medicine2021

The IL-33/ST2 axis affects tumor growth by regulating mitophagy in macrophages and reprogramming their polarization.

Huadan Xu, Dong Li, Jiaoyan Ma, Yuanxin Zhao, Long Xu, Rui Tian, Yanan Liu, Liankun Sun, Jing Su

Open access · goldAbstract read
In one paragraph

Article in Cancer biology & medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

27 citing papers in PubMed, 42 citations in OpenAlex.

  1. Review
  2. Advances in understanding mitophagy's role in lung injury.Chinese journal of traumatology = Zhonghua chuang shang za zhi · 2026
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  17. Innovation (Cambridge (Mass.)) · 2023
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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

9 authors at 2 institutions in 1 country.

Huadan XuKey Laboratory of Pathobiology, Ministry of Education, Department of Pathophysiology, College of Basic Medical Sciences, Jilin University, Changchun 130000, China.
Dong LiDepartment of Hepatology, The First Hospital of Jilin University, Changchun 130000, China.
Jiaoyan MaKey Laboratory of Pathobiology, Ministry of Education, Department of Pathophysiology, College of Basic Medical Sciences, Jilin University, Changchun 130000, China.
Yuanxin ZhaoKey Laboratory of Pathobiology, Ministry of Education, Department of Pathophysiology, College of Basic Medical Sciences, Jilin University, Changchun 130000, China.
Long XuKey Laboratory of Pathobiology, Ministry of Education, Department of Pathophysiology, College of Basic Medical Sciences, Jilin University, Changchun 130000, China.
Rui TianKey Laboratory of Pathobiology, Ministry of Education, Department of Pathophysiology, College of Basic Medical Sciences, Jilin University, Changchun 130000, China.
Yanan LiuKey Laboratory of Pathobiology, Ministry of Education, Department of Pathophysiology, College of Basic Medical Sciences, Jilin University, Changchun 130000, China.
Liankun SunKey Laboratory of Pathobiology, Ministry of Education, Department of Pathophysiology, College of Basic Medical Sciences, Jilin University, Changchun 130000, China.ORCID 0000-0003-0560-1238
Jing SuKey Laboratory of Pathobiology, Ministry of Education, Department of Pathophysiology, College of Basic Medical Sciences, Jilin University, Changchun 130000, China.ORCID 0000-0001-7636-2946
Jilin University · CNFirst Hospital of Jilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objective: Macrophages are a major component of the tumor microenvironment. M1 macrophages secrete pro-inflammatory factors that inhibit tumor growth and development, whereas tumor-associated macrophages (TAMs) mainly exhibit an M2 phenotype. Our previous studies have shown that the interleukin-33/ST2 (IL-33/ST2) axis is essential for activation of the M1 phenotype. This study investigates the role of the IL-33/ST2 axis in TAMs, its effects on tumor growth, and whether it participates in the mutual conversion between the M1 and M2 phenotypes. Methods: Bone marrow-derived macrophages were extracted from wildtype, ST2 knockout (ST2 Results: The IL-33/ST2 axis was demonstrated to play an important role in the metabolic conversion of macrophages from OXPHOS to glycolysis by altering mitophagy levels. The IL-33/ST2 axis promoted enhanced cell oxidative phosphorylation, thereby further increasing M2 polarization gene expression and ultimately promoting tumor growth ( Conclusions: These results clarify the interaction between the IL-33/ST2 pathway and macrophage polarization, and may pave the way to the development of new cancer immunotherapies targeting the IL-33/ST2 axis.

Indexed as

MitophagyAnimalsCell DifferentiationInterleukin-1 Receptor-Like 1 ProteinInterleukin-33Macrophage ActivationMacrophagesMaleMiceMice, Inbred BALB CMitochondriaNeoplasmsOxidative PhosphorylationPhenotypeTOR Serine-Threonine KinasesTumor MicroenvironmentIl1rl1 protein, mouseIl33 protein, mouseInterleukin-1 Receptor-Like 1 ProteinInterleukin-33TOR Serine-Threonine Kinasesglucose metabolismIL-33/ST2macrophage polarizationmitophagytumor microenvironment

Identifiers

PMID33628592
PMCPMC7877183
OpenAlexW3088450227

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Registered trials

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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.