Evidence map›Paper›PMID 35855866›Full record

ArticleOxidative medicine and cellular longevity2022

lncRNA PINK1-AS Aggravates Cerebral Ischemia/Reperfusion Oxidative Stress Injury through Regulating ATF2 by Sponging miR-203.

Zhong-Bao Yang, Yu Xiang, Mei-Lin Zuo, Li Mao, Guo-Huang Hu, Gui-Lin Song, Md Sayed Ali Sheikh, Li-Ming Tan

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

10 citing papers in PubMed, 13 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

8 authors at 3 institutions in 2 countries.

Zhong-Bao YangThe Affiliated Changsha Hospital of Hunan Normal University, Changsha, Hunan 410006, China.ORCID https://orcid.org/0000-0002-1334-8386
Yu XiangThe Affiliated Changsha Hospital of Hunan Normal University, Changsha, Hunan 410006, China.
Mei-Lin ZuoThe Affiliated Changsha Hospital of Hunan Normal University, Changsha, Hunan 410006, China.
Li MaoDepartment of Basic Medicine, Changsha Health Vocational College, Changsha, Hunan 410600, China.
Guo-Huang HuThe Affiliated Changsha Hospital of Hunan Normal University, Changsha, Hunan 410006, China.
Gui-Lin SongThe Affiliated Changsha Hospital of Hunan Normal University, Changsha, Hunan 410006, China.
Md Sayed Ali SheikhInternal Medicine Department, Cardiology, College of Medicine, Jouf University, Sakaka, Aljouf, 72338¸, Saudi Arabia.
Li-Ming TanThe Affiliated Changsha Hospital of Hunan Normal University, Changsha, Hunan 410006, China.ORCID https://orcid.org/0000-0002-4304-1211
Hunan Normal University · CNChangsha Hospital for Maternal and Child Health Care · CNJouf University · SA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ischemic stroke is a common disease that led to high mortality and high disability. NADPH oxidase 2- (NOX2-) mediated oxidative stress and long noncoding RNA have important roles in cerebral ischemia/reperfusion (CI/R) injury, whereas whether there is interplay between them remains to be clarified. This study was performed to observe the role of lncRNA PINK1-antisense RNA (PINK1-AS) in NOX2 expression regulation. An in vivo rat model (MCAO) and an in vitro cell model (H/R: hypoxia/reoxygenation) were utilized for CI/R oxidative stress injury investigation. The expression levels of lncRNA PINK1-AS, activating transcription factor 2 (ATF2), NOX2, and caspase-3 and the production level of ROS and cell apoptosis were significantly increased in CI/R injury model rats or in H/R-induced SH-SY5Y cells, but miR-203 was significantly downregulated. There was positive correlation between PINK1-AS expression level and ROS production level. PINK1-AS and ATF2 were found to be putative targets of miR-203. Knockdown of lncRNA PINK1-AS or ATF2 or the overexpression of miR-203 significantly reduced oxidative stress injury via inhibition of NOX2. Overexpression of lncRNA PINK1 significantly led to oxidative stress injury in SH-SY5Y cells through downregulating miR-203 and upregulating ATF2 and NOX2. lncRNA PINK1-AS and ATF2 were the targets of miR-203, and the lncRNA PINK1-AS/miR-203/ATF2/NOX2 axis plays pivotal roles in CI/R injury. Therefore, lncRNA PINK1-AS is a possible target for CR/I injury therapy by sponging miR-203.

Indexed as

Activating Transcription Factor 2Brain IschemiaMicroRNAsReperfusion InjuryRNA, Long NoncodingAnimalsApoptosisCerebral InfarctionHumansNeuroblastomaOxidative StressProtein KinasesRatsReactive Oxygen SpeciesActivating Transcription Factor 2ATF2 protein, humanAtf2 protein, ratMicroRNAsMIRN203 microRNA, humanMIRN203 microRNA, ratProtein KinasesReactive Oxygen SpeciesRNA, Long Noncoding

Identifiers

PMID35855866
PMCPMC9288285
OpenAlexW4284959995

What Socratic holds

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LicenceCC BY
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Registered trials

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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 Socratic graph.