Evidence map›Paper›PMID 31858374›Full record

ArticleNeurochemical research2020

Silencing of TXNIP Alleviated Oxidative Stress Injury by Regulating MAPK-Nrf2 Axis in Ischemic Stroke.

Yu Tian, Yue Su, Qile Ye, Lei Chen, Fei Yuan, Zhenyu Wang

Registry-linked trialAbstract read
PubMed Publisher
In one paragraph

Article in Neurochemical research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07626541 (Clinical Study of Fructose Injection in the Treatment of Acute Ischemic Stroke), which is not on this map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.8field-weighted citation impact, top 14% 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.

NCT07626541 phase2active not recruitingnot on this mapstarted 2026, after this paper: background citation

Clinical Study of Fructose Injection in the Treatment of Acute Ischemic Stroke

TypeinterventionalSponsorJi Xunming,MD,PhDRan2026 to 2026Enrolled46ConditionsAcute Ischemic StrokeArms10% Fructose Injection
3 · Its place in the literature

Who cites it

23 citing papers in PubMed, 40 citations in OpenAlex.

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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

6 authors at 1 institution in 1 country.

Yu TianDepartment of Neurosurgery, The 2nd Affiliated Hospital of Harbin Medical University, Harbin, 150086, China.
Yue SuFunctional Experimental Teaching Center, College of Basic Medical Sciences, Harbin Medical University, Harbin, 150086, China.
Qile YeDepartment of Neurosurgery, The 2nd Affiliated Hospital of Harbin Medical University, Harbin, 150086, China.
Lei ChenDepartment of Neurosurgery, The 2nd Affiliated Hospital of Harbin Medical University, Harbin, 150086, China.
Fei YuanDepartment of Neurosurgery, The 2nd Affiliated Hospital of Harbin Medical University, Harbin, 150086, China.
Zhenyu WangDepartment of Neurosurgery, The 2nd Affiliated Hospital of Harbin Medical University, Harbin, 150086, China. 373259629@qq.com.ORCID http://orcid.org/0000-0001-8379-4288
Harbin Medical University · CN

Funding

Heilongjiang Provincial Postdoctoral Science Foundation LBH-Z18175
6 · The paper itself

Abstract

Ischemic stroke is a life-threatening cerebrovascular thrombotic disease, oxidative stress is considered to be a critical factor to stroke pathophysiology. This study aimed to investigate the underlying molecular mechanism and propose the potential therapeutic strategy for ischemic stroke. Bioinformatics analysis based on a public microarray profile (GSE 61616) of ischemic stroke rats was performed as a pilot research. Oxidative stress was enriched as a significantly gene ontology item, and thioredoxin-interacting protein (TXNIP) and MAPK signaling were identified as the hub gene and pathway, respectively. The experiments in middle cerebral artery occlusion rats demonstrated that ischemia induced the activation of oxidative stress. The expressions of TXNIP, p-p38, p-JNK, p-ERK were significantly increased while Nrf2 and HO-1 expressions were decreased after stroke. Rescue assays were conducted in primary cultured neurons to explore the accurate interrelations among these factors. The results indicated that MAPK specific inhibitor and siRNA-TXNIP significantly alleviated the oxidative stress injury induced by oxygen-glucose deprivation. In addition, knocking down of TXNIP inhibited the activation of MAPK pathway and promoted Nrf2 pathway. Taken together, these findings indicated that TXNIP aggravated the oxidative stress injury by regulating MAPK-Nrf2 axis in ischemic stroke. Silencing of TXNIP seems a promising therapeutic strategy to alleviate ischemic stroke.

Indexed as

AnimalsCell Cycle ProteinsInfarction, Middle Cerebral ArteryMaleMAP Kinase Signaling SystemOxidative StressRats, Sprague-DawleyRNA, Small InterferingUp-RegulationCell Cycle ProteinsRNA, Small InterferingTXNIP protein, ratIschemic strokeMAPK signalingOxidative stressThioredoxin-interacting protein

Identifiers

PMID31858374
OpenAlexW2996143879

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.