Evidence map›Paper›PMID 31929494›Full record

ArticleMedical science monitor : international medical journal of experimental and clinical research2020

The Nephroprotective Effect of TNF Receptor-Associated Factor 6 (TRAF6) Blockade on LPS-Induced Acute Renal Injury Through the Inhibition if Inflammation and Oxidative Stress.

Xuemei Chen, Yiqing Zhao, Jiajun Xu, Jiachun Bao, Junyao Zhao, Jingfeng Chen, Guowei Chen, Jibo Han

RetractedOpen access · hybridAbstract readRetracted Publication
In one paragraph

Article in Medical science monitor : international medical journal of experimental and clinical research, 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 It has been retracted, and should not be counted.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 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

5 citing papers in PubMed, 6 citations in OpenAlex.

  1. Extracellular vesicles derived from inflammatory-educated stem cells reverse brain inflammation-implication of miRNAs.Molecular therapy : the journal of the American Society of Gene Therapy · 2022
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 1 country.

Xuemei ChenDepartment of Pharmacy, Affiliated Hospital of Jiangnan University, Wuxi, Jiangsu, China (mainland).
Yiqing ZhaoDepartment of Pharmacy, Affiliated Hospital of Jiangnan University, Wuxi, Jiangsu, China (mainland).
Jiajun XuDepartment of Cardiology, The Second Affiliated Hospital of Jiaxing University, Jiaxing, Zhejiang, China (mainland).
Jiachun BaoDepartment of Pharmacy, Affiliated Hospital of Jiangnan University, Wuxi, Jiangsu, China (mainland).
Junyao ZhaoDepartment of Pharmacy, Affiliated Hospital of Jiangnan University, Wuxi, Jiangsu, China (mainland).
Jingfeng ChenDepartment of Pharmacy, Affiliated Hospital of Jiangnan University, Wuxi, Jiangsu, China (mainland).
Guowei ChenDepartment of Cardiology, The Second Affiliated Hospital of Jiaxing University, Jiaxing, Zhejiang, China (mainland).
Jibo HanDepartment of Cardiology, The Second Affiliated Hospital of Jiaxing University, Jiaxing, Zhejiang, China (mainland).
Jiaxing University · CNWuxi Fourth People's Hospital · CNJiangnan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND Inflammation and oxidative stress play important roles in the pathogenesis of acute kidney injury (AKI). TRAF6 functions as a signal transducer in the Toll-like receptor 4 signaling pathway. Several reports have previously implicated TRAF6 signaling in kidney pathology. Here, we investigated whether TRAF6 blockade can mitigate inflammatory responses and oxidative stress in AKI. MATERIAL AND METHODS C57BL/6 mice were injected with lipopolysaccharide (LPS, 15 mg/kg) to induce AKI. Double immunofluorescence staining of kidney tissues showed that TRAF6 was localized to renal tubular epithelial cells, and then a tubular epithelial cell line (NRK-52E) was used for in vitro analysis. TRAF6 was blocked in vitro using siRNA and in vivo using AAV2/2 shRNA. RESULTS The knockdown of TRAF6 in mice by AAV2-shTRAF6 significantly reduced renal inflammation, oxidative stress, apoptosis and kidney dysfunction in AKI. In vitro, silencing the expression of TRAF6 attenuated LPS(0.5 μg/mL)-induced inflammatory responses and oxidative stress and upregulated proapoptotic factors. Furthermore, the beneficial actions of TRAF6 blockade were closely associated with its ability to increase IkappaB-alpha and Nrf2. CONCLUSIONS Our findings provide direct evidence that TRAF6 mediates LPS-induced inflammation and oxidative stress, leading to renal dysfunction. We also show that TRAF6 inhibition is a potential therapeutic option to prevent AKI.

Indexed as

Oxidative StressAcute Kidney InjuryAnimalsApoptosisEpithelial CellsFibrosisGene Knockdown TechniquesGene SilencingInflammationKidney TubulesLipopolysaccharidesMaleMice, Inbred C57BLNF-E2-Related Factor 2NF-KappaB Inhibitor alphaProtective AgentsLipopolysaccharidesNfe2l2 protein, mouseNF-E2-Related Factor 2NF-KappaB Inhibitor alphaProtective AgentsRNA, Small InterferingTNF Receptor-Associated Factor 6

Identifiers

PMID31929494
PMCPMC6977635
OpenAlexW2999984571

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.