Evidence map›Paper›PMID 39921798›Full record

ArticleCardiovascular toxicology2025

TRIM21 Promotes Endothelial Cell Activation via Accelerating SOCS3 Ubiquitination Degradation in Atherosclerosis.

Zhenxuan Hao, Yihuan Wang, Linlin Chen, Yanjun Zhou, Dezhou Fang, Wenxiang Yao, Lili Xiao, Yanzhou Zhang

Abstract read
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In one paragraph

Article in Cardiovascular toxicology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

8 authors.

Zhenxuan Hao *Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou, 450052, Henan, China.
Yihuan Wang *Department of Emergency, The First Affiliated Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou, 450052, Henan, China.
Linlin ChenDepartment of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou, 450052, Henan, China.
Yanjun ZhouDepartment of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou, 450052, Henan, China.
Dezhou FangDepartment of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou, 450052, Henan, China.
Wenxiang YaoDepartment of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou, 450052, Henan, China.
Lili XiaoDepartment of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou, 450052, Henan, China. xll0827@126.com.
Yanzhou ZhangDepartment of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou, 450052, Henan, China. fcczhangyz@zzu.edu.cn.

Funding

Scientific Research and Innovation Team of The FirstAffiliated Hospital of ZhengzhouUniversity ZYCXTD2023016
6 · The paper itself

Abstract

Activated endothelial cells play an important role in the beginning of atherosclerotic disease by secreting various proteins and inflammatory cytokines. Ubiquitination is one of the most common post-translational changes in cells. However, the role and mechanisms of ubiquitination in endothelial cell activation remain poorly understood. In this study, we identified TRIM21 as an E3 ubiquitin ligase with increased expression in atherosclerotic disease and activated endothelial cells. Knockdown of TRIM21 resulted in reduced secretion of inflammatory factors and attenuated the pyroptosis of endothelial cells, inhibiting the progression of atherosclerosis. Mechanistically, TRIM21 could bind and ubiquitinate SOCS3, thereby enhancing NLRP3-mediated pyroptosis. Taken together, we found that endothelial TRIM21 activated the JAK/STAT3 pathway by degrading SOCS3, which in turn promoted NLRP3-mediated pyroptosis and aggravated atherosclerosis, revealing that TRIM21 may be a promising treatment target for the medical management of atherosclerosis.

Indexed as

AtherosclerosisEndothelial CellsHuman Umbilical Vein Endothelial CellsInflammasomesRibonucleoproteinsSuppressor of Cytokine Signaling 3 ProteinAnimalsCells, CulturedDisease Models, AnimalHumansInflammation MediatorsMaleMice, Inbred C57BLNLR Family, Pyrin Domain-Containing 3 ProteinPlaque, AtheroscleroticProteolysisInflammasomesInflammation MediatorsNLR Family, Pyrin Domain-Containing 3 ProteinRibonucleoproteinsSOCS3 protein, humanSS-A AntigenSTAT3 protein, humanSTAT3 Transcription FactorSuppressor of Cytokine Signaling 3 ProteinAtherosclerosisEndothelial cellPyroptosisSOCS3TRIM21

Identifiers

PMID39921798

What OpenQuestion holds

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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.