Evidence map›Paper›PMID 35094204›Full record

ArticleCellular and molecular life sciences : CMLS2022

Thioredoxin reductase 3 suppression promotes colitis and carcinogenesis via activating pyroptosis and necrosis.

Qi Liu, Pengyue Du, Yue Zhu, Xintong Zhang, Jingzeng Cai, Ziwei Zhang

Open access · greenAbstract read
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2022. 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
6.6field-weighted citation impact, top 2% 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, 61 citations in OpenAlex.

  1. Review
  2. The protective effects of selenium against NLRP3-mediated inflammation and pyroptosis: mechanisms and the potential health benefits.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026
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  15. STIM1 in tumor cell death: angel or devil?Cell death discovery · 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

6 authors at 1 institution in 1 country.

Qi LiuCollege of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, People's Republic of China.
Pengyue DuCollege of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, People's Republic of China.
Yue ZhuCollege of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, People's Republic of China.
Xintong ZhangCollege of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, People's Republic of China.
Jingzeng CaiCollege of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, People's Republic of China.
Ziwei ZhangCollege of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, People's Republic of China. zhangziwei@neau.edu.cn.ORCID http://orcid.org/0000-0002-5705-4611
Northeast Agricultural University · CN

Funding

National Natural Science Foundation of China 31872531
6 · The paper itself

Abstract

backgroundTxnrd3 as selenoprotein plays key roles in antioxidant process and sperm maturation. Inflammatory bowel diseases, such as ulcerative colitis and Crohn's disease, are becoming significantly increasing disease worldwide in recent years which are proved relative to diet, especially selenium intake.

methodsIn the present study, 8-week-old C57BL/6N male Txnrd3-/-, Txnrd3-/ + , Txnrd3 + / + mice, weight 25-30 g, were randomly chosen and each group with 30 mice. Feed 3.5% DSS drinking water and normal water continuously for 7 days. Mouse colon cancer cells (CT26) were cultured in vitro to establish Txnrd3 overexpressed/knocked-down model by cell transfection technology. Morphology and ultrastructure, calcium levels, ROS level, cell death were observed and detected in vivo and vitro.

resultsIn Txnrd3-/-mice, ulcerative colitis was more severe, the morphological and ultrastructural lesions were also more prominent compared with wild-type mice, accompanied by the significantly increased expression of NLRP3, Caspase1, RIPK3, and MLKL. Overexpression of Txnrd3 could lead to increased oxidative stress through intracellular calcium outflow-induced oxidative stress increase followed by necrosis and pyroptosis pathway activation and further inhibit the growth and proliferation of colon cancer cells.

conclusionTxnrd3 overexpression leads to intracellular calcium outflow and increased ROS, which eventually leads to necrosis and focal death of colon cancer cells, while causing Txnrd3-/- mice depth of the crypt deeper, weakened intestinal secretion and immune function and aggravate the occurrence of ulcerative colitis. The present study lays a foundation for the prevention and treatment of ulcerative colitis and colon carcinoma in clinic treatment.

Indexed as

Disease Models, AnimalAnimalsCalciumCarcinogenesisCaspase 1Cell Line, TumorCell ProliferationColitis, UlcerativeColonDextran SulfateGene ExpressionHumansMaleMiceMice, Inbred C57BLMice, KnockoutCalciumCaspase 1Dextran SulfateReactive Oxygen SpeciesThioredoxin-Disulfide ReductaseTxnrd3 protein, mouseC57BL/6NColon cancerOxidative stressTxnrd3Ulcerative colitis

Identifiers

PMID35094204
PMCPMC11072778
OpenAlexW4220733997

What OpenQuestion holds

Textmetadata
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.