Evidence map›Paper›PMID 31676570›Full record

ArticleRNA (New York, N.Y.)2020

MiR-146a down-regulates inflammatory response by targeting TLR3 and TRAF6 in Coxsackievirus B infection.

Yanru Fei, Anita Chaulagain, Tianying Wang, Yang Chen, Jinchang Liu, Ming Yi, Ying Wang, Yike Huang, Lexun Lin, Sijia Chen and 7 more

Open access · bronzeAbstract read
In one paragraph

Article in RNA (New York, N.Y.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

26 citing papers in PubMed, 37 citations in OpenAlex.

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  10. MiRNA-146a-A Key Player in Immunity and Diseases.International journal of molecular sciences · 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

17 authors at 1 institution in 1 country.

Yanru FeiDepartment of Microbiology, Harbin Medical University, Harbin 150081, China.
Anita ChaulagainDepartment of Microbiology, Harbin Medical University, Harbin 150081, China.
Tianying WangDepartment of Microbiology, Harbin Medical University, Harbin 150081, China.
Yang ChenDepartment of Microbiology, Harbin Medical University, Harbin 150081, China.
Jinchang LiuDepartment of Microbiology, Harbin Medical University, Harbin 150081, China.
Ming YiDepartment of Microbiology, Harbin Medical University, Harbin 150081, China.
Ying WangDepartment of Microbiology, Harbin Medical University, Harbin 150081, China.
Yike HuangDepartment of Cell Biology, Harbin Medical University, Harbin 150081, China.
Lexun LinDepartment of Microbiology, Harbin Medical University, Harbin 150081, China.
Sijia ChenDepartment of Microbiology, Harbin Medical University, Harbin 150081, China.
Weizhen XuDepartment of Microbiology, Harbin Medical University, Harbin 150081, China.
Lei TongDepartment of Microbiology, Harbin Medical University, Harbin 150081, China.
Xiaoyu WuDepartment of Cardiology, The First Hospital of Harbin Medical University, Harbin 150001, China.
Dechao ZhaoDepartment of Cardiology, The First Hospital of Harbin Medical University, Harbin 150001, China.
Fengmin ZhangDepartment of Microbiology, Harbin Medical University, Harbin 150081, China.
Wenran ZhaoDepartment of Cell Biology, Harbin Medical University, Harbin 150081, China.
Zhaohua ZhongDepartment of Microbiology, Harbin Medical University, Harbin 150081, China.
Harbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Coxsackievirus B (CVB) is the major cause of human myocarditis and dilated cardiomyopathy. Toll-like receptor 3 (TLR3) is an intracellular sensor to detect pathogen's dsRNA. TLR3, along with TRAF6, triggers an inflammatory response through NF-κB signaling pathway. In the cells infected with CVB type 3 (CVB3), the abundance of miR-146a was significantly increased. The role of miR-146a in CVB infection is unclear. In this study, TLR3 and TRAF6 were identified as the targets of miR-146a. The elevated miR-146a inhibited NF-κB translocation and subsequently down-regulated proinflammatory cytokine expression in the CVB3-infected cells. Therefore, the NF-κB pathway can be doubly blocked by miR-146a through targeting of TLR3 and TRAF6. MiR-146a may be a negative regulator on inflammatory response and an intrinsic protective factor in CVB infection.

Indexed as

Signal TransductionAnimalsCoxsackievirus InfectionsCytokinesDown-RegulationEnterovirus B, HumanFibroblastsHeLa CellsHumansInflammationIntracellular Signaling Peptides and ProteinsMiceMice, Inbred BALB CMicroRNAsNF-kappa BToll-Like Receptor 3CytokinesIntracellular Signaling Peptides and ProteinsMicroRNAsMIRN146 microRNA, humanNF-kappa BTifab protein, humanTLR3 protein, humanToll-Like Receptor 3Coxsackievirus BmiR-146aNF-κBTLR3TRAF6

Identifiers

PMID31676570
PMCPMC6913124
OpenAlexW2984658254

What OpenQuestion holds

Textmetadata
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.