Evidence map›Paper›PMID 23029542›Full record

ArticlePloS one2012

A20 (TNFAIP3) alleviates CVB3-induced myocarditis via inhibiting NF-κB signaling.

Jun Gui, Yan Yue, Ruizhen Chen, Wei Xu, Sidong Xiong

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

36 citing papers in PubMed, 120 citations in OpenAlex.

  1. Article
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  4. Article
  5. Roles of inflammasomes in viral myocarditis.Frontiers in cellular and infection microbiology · 2023
    Review
  6. Cardiac-specific ITCH overexpression ameliorates septic cardiomyopathyJournal of molecular and cellular cardiology plus · 2022
    Article
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  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. A20 alleviates the vascular remodeling induced by homocysteine.American journal of translational research · 2018
    Article
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

5 authors at 3 institutions in 1 country.

Jun GuiInstitute for Immunobiology, Shanghai Medical College, Fudan University, Shanghai, People's Republic of China.
Yan Yue
Ruizhen Chen
Wei Xu
Sidong Xiong
Soochow University · CNShanghai Medical College of Fudan University · CNZhongshan Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundViral myocarditis, which is most prevalently caused by Coxsackievirus B3 (CVB3) infection, is a serious clinical condition characterized by cardiac inflammation. However, efficient therapies targeting inflammation are still lacking and much needed. A20, also known as tumor necrosis factor alpha induced protein 3 (TNFAIP3) is a key negative regulator of inflammation. But whether A20 may affect cardiac inflammation during acute viral myocarditis remains to be elucidated. The aim of this study was to investigate the potential protective effect of A20 on CVB3-induced myocarditis. METHODOLOGY/PRINCIPAL

findingsMice were intraperitoneally inoculated with CVB3 to establish acute viral myocarditis model. We found that the expression of pro-inflammatory cytokines, including tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-6 and monocyte chemotactic protein-1 (MCP-1) were markedly and persistently increased during the progression of CVB3-induced myocarditis, and positively correlated with the disease severity. Notably, intravenous injection in vivo with adenovirus expressed A20 (Ad-A20) remarkably reduced CVB3-induced pro-inflammatory cytokines production and alleviated the severity of myocarditis. Further, we observed that nuclear factor-kappaB (NF-κB) signaling which mediates inflammatory response was significantly inhibited in CVB3-infected mice with Ad-A20 treatment. Finally, we revealed that A20 was required to inhibit CVB3-induced NF-κB signaling by restricting TNF receptor associated factor 6 (TRAF6) ubiquitylation. CONCLUSION/SIGNIFICANCE: This study demonstrates the protective role of A20 against CVB3-induced myocarditis, which may provide a new therapeutic strategy for the treatment of viral myocarditis.

Indexed as

Enterovirus B, HumanAdenoviridaeAnimalsCells, CulturedCoxsackievirus InfectionsCysteine EndopeptidasesCytokinesGenetic VectorsIntracellular Signaling Peptides and ProteinsMaleMiceMice, Inbred BALB CMyocarditisMyocardiumMyocytes, CardiacNF-kappa BCysteine EndopeptidasesCytokinesIntracellular Signaling Peptides and ProteinsNF-kappa BRecombinant ProteinsTnfaip3 protein, mouseTNF Receptor-Associated Factor 6Tumor Necrosis Factor alpha-Induced Protein 3

Identifiers

PMID23029542
PMCPMC3460927
OpenAlexW2038999893

What OpenQuestion holds

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LicenceCC BY
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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.