Evidence map›Paper›PMID 32893965›Full record

ArticleThoracic cancer2020

Glutaredoxin 1 regulates macrophage polarization through mediating glutathionylation of STAT1.

Lijuan Guo, Shanze Chen, Qingrong Liu, Hongyu Ren, Yuhao Li, Junyue Pan, Yuhan Luo, Tongzhou Cai, Ruofan Liu, Junli Chen and 4 more

Open access · goldAbstract read
In one paragraph

Article in Thoracic cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.5field-weighted citation impact, top 37% 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

10 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. A Prognostic Activity of Glutaredoxin 1 Protein (Grx1) in Colon Cancer.International journal of molecular sciences · 2024
    Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Review
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

14 authors at 2 institutions in 1 country.

Lijuan GuoDepartment of Pathophysiology, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, China.
Shanze ChenDepartment of Pathophysiology, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, China.
Qingrong LiuDepartment of Pathophysiology, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, China.
Hongyu RenDepartment of Pathophysiology, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, China.
Yuhao LiDepartment of Pathophysiology, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, China.
Junyue PanDepartment of Pathophysiology, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, China.
Yuhan LuoDepartment of Pathophysiology, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, China.
Tongzhou CaiDepartment of Pathophysiology, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, China.
Ruofan LiuDepartment of Pathophysiology, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, China.
Junli ChenDepartment of Pathophysiology, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, China.
Yi WangDepartment of Pathophysiology, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, China.
Xiaoying WangDepartment of Pathophysiology, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, China.
Ning HuangDepartment of Pathophysiology, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, China.
Jingyu LiDepartment of Pathophysiology, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, China.ORCID 0000-0003-0997-9115
West China Medical Center of Sichuan University · CNJinan University · CN

Funding

National Natural Science Foundation of China 31401188National Natural Science Foundation of China 81470931Science Foundation for Excellent Youth Scholars of Sichuan University Grant 2016SCU04A08Sichuan Association for Science and Technology 2018RCTJ04Undergraduate Innovation and Entrepreneurship Training Program for Sichuan University C2019106935Undergraduate Innovation and Entrepreneurship Training Program for Sichuan University C2020113908
6 · The paper itself

Abstract

backgroundMacrophage polarization affects tumor growth, metabolism, and many other tumor processes. M1 macrophages can promote antitumor immunity response. Signal transducer and activator of transcription 1 (STAT1) is one of the critical transcription factors in this process, which promotes the expression of a series of inflammatory molecules. STAT1 has been reported as a potential target of reactive oxygen species (ROS)-induced glutathionylation, while the glutathionylation of STAT1 in macrophages and its underlying regulatory mechanism remains unclear. Glutaredoxin 1 (Grx1) functions as a deglutathionylation enzyme, which regulates the activities of many proteins through reversing glutathionylation.

methodsGeneChip and RT-qPCR was first applied to test the mRNA level of Grx1 in M1 macrophages. Western blot was then used to evaluate the variations of the Grx1 protein expression in M1 macrophages. Next, immunoprecipitation was used to investigate the glutathionylated STAT1 in both wild-type and Grx1

resultsIn M1-type macrophages, the levels of Grx1 were elevated. Glutathionylation of STAT1 was negatively regulated by Grx1. Furthermore, depletion of Grx1 increased the activity of STAT1, and thereby promoted the mRNA level of C-X-C motif chemokine ligand 9 (CXCL9) during M1-type polarization of macrophages.

conclusionsGrx1 controlled deglutathionylation of STAT1, which in turn might regulate M1-type polarization of macrophages.

Indexed as

AnimalsCell PolarityGlutaredoxinsMacrophagesMiceMice, Inbred C57BLRAW 264.7 CellsSTAT1 Transcription FactorGlrx protein, mouseGlutaredoxinsStat1 protein, mouseSTAT1 Transcription FactorGlutaredoxinglutathionylationmacrophage polarizationSTAT1

Identifiers

PMID32893965
PMCPMC7529579
OpenAlexW3084348434

What OpenQuestion holds

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LicenceCC BY-NC
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.