Evidence map›Paper›PMID 32346399›Full record

ArticleGut pathogens2020

EV71 virus reduces Nrf2 activation to promote production of reactive oxygen species in infected cells.

Zhenzi Bai, Xiaonan Zhao, Chenghua Li, Chuanlun Sheng, Hongyan Li

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in Gut pathogens, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
4.2field-weighted citation impact, top 4% 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

15 citing papers in PubMed, 32 citations in OpenAlex.

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  14. NRF2 in Viral Infection.Antioxidants (Basel, Switzerland) · 2021
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Zhenzi Bai *Infectious Department, China-Japan Union Hospital, Jilin University, No.126, Xiantai Street, Economic Development Zone, Changchun, 130033 Jilin China.
Xiaonan Zhao *Infectious Department, China-Japan Union Hospital, Jilin University, No.126, Xiantai Street, Economic Development Zone, Changchun, 130033 Jilin China.
Chenghua LiInfectious Department, China-Japan Union Hospital, Jilin University, No.126, Xiantai Street, Economic Development Zone, Changchun, 130033 Jilin China.
Chuanlun ShengInfectious Department, China-Japan Union Hospital, Jilin University, No.126, Xiantai Street, Economic Development Zone, Changchun, 130033 Jilin China.
Hongyan LiInfectious Department, China-Japan Union Hospital, Jilin University, No.126, Xiantai Street, Economic Development Zone, Changchun, 130033 Jilin China.
Union Hospital · CNJilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEmerging evidence closely links Enterovirus 71 (EV71) infection with the generation of reactive oxygen species (ROS). Excess ROS results in apoptosis and exacerbates inflammatory reactions. The Keap1-Nrf2 axis serves as an essential oxidant counteracting pathway.

methodsThe present study aimed to elucidate the role of the Keap1-Nrf2 pathway in modulating apoptosis and inflammatory reactions triggered by oxidative stress in Vero and RD cells upon EV71 infection.

resultsElevated ROS production was identified in EV71 infected Vero and RD cells. The percentage of dead cells and expression of inflammation-promoting cytokines were increased in these cells. EV71 infected cells also displayed reinforced Keap1 expression and abrogated Nrf2 expression. Keap1 silencing resulted in the downstream aggregation of the Nrf2 protein and heme oxygenase-1 HO-1. Keap1 silencing repressed ubiquitination and reinforced Nrf2 nuclear trafficking. Furthermore, silencing Keap1 expression repressed ROS production, cell death, and inflammatory reactions in EV71 infected RD and Vero cells. In contrast, silencing of both Keap1 and Nrf2 restored ROS production, cell death, and inflammatory reactions. Nrf2 and Keap1 modulated the stimulation of the Akt sensor and extrinsic as well as intrinsic cell death pathways, resulting in EV71-triggered cell death and inflammatory reactions.

conclusionsEV71 infection can trigger ROS production, cell death, and inflammatory reactions by modulating the Nrf2 and Keap1 levels of infected cells.

Indexed as

ApoptosisEV71 virusInflammationKeap1Nrf2ROS

Identifiers

PMID32346399
PMCPMC7181592
OpenAlexW3018403976

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.