Evidence map›Paper›PMID 28871076›Full record

ArticleMedical science monitor : international medical journal of experimental and clinical research2017

Knockdown of MicroRNA-122 Protects H9c2 Cardiomyocytes from Hypoxia-Induced Apoptosis and Promotes Autophagy.

Zaiwei Zhang, Hu Li, Shasha Chen, Ying Li, Zhiyuan Cui, Jie Ma

RetractedOpen access · greenAbstract readRetracted Publication
In one paragraph

Article in Medical science monitor : international medical journal of experimental and clinical research, 2017. 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 It has been retracted, and should not be counted.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 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

32 citing papers in PubMed, 55 citations in OpenAlex.

  1. Review
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  6. Retracted: Knockdown of MicroRNA-122 Protects H9c2 Cardiomyocytes from Hypoxia-Induced Apoptosis and Promotes Autophagy.Medical science monitor : international medical journal of experimental and clinical research · 2021
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  13. Therapeutic Value of miRNAs in Coronary Artery Disease.Oxidative medicine and cellular longevity · 2021
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors.

Zaiwei ZhangDepartment of Cardiovascular Medicine, Jining No.1 People's Hospital, Jining, Shandong, China (mainland).
Hu LiDepartment of Cardiovascular Medicine, Jining No.1 People's Hospital, Jining, Shandong, China (mainland).
Shasha ChenDepartment of Cardiovascular Medicine, Jining No.1 People's Hospital, Jining, Shandong, China (mainland).
Ying LiDepartment of Cardiovascular Medicine, Jining No.1 People's Hospital, Jining, Shandong, China (mainland).
Zhiyuan CuiDepartment of Cardiovascular Medicine, Jining No.1 People's Hospital, Jining, Shandong, China (mainland).
Jie MaDepartment of Cardiovascular Medicine, Jining No.1 People's Hospital, Jining, Shandong, China (mainland).

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND Acute myocardial infarction (AMI) is a severe disease causing heart failure and sudden death. Studies indicate that microRNAs (miRNAs) are involved in the pathophysiology of AMI. In the present study, we carefully explored the effects of miR-122 on myocardial hypoxia injury and its possible underlying mechanism. MATERIAL AND METHODS miR-122 expression was analyzed in H9c2 cardiomyocytes after being transfected with miR-122 mimic, ASO-miR-122, or negative control. Cell viability and apoptosis were investigated by CCK-8 assays and flow cytometry analysis, respectively. Cell migration was analyzed using wound-healing assays. Western blotting was performed to analyze the expression of phosphatase and tensin homolog deleted on chromosome 10 (PTEN)/phosphatidylinositol 3-hydroxy kinase (PI3K)/AKT and LC3-II/LC3-I. RESULTS Hypoxia exposure significantly inhibited H9c2 cell viability (P<0.01). miR-122 overexpression promoted the hypoxia-induced H9c2 cell proliferation and migration loss (P<0.05), and cell apoptosis was increased (P<0.05). miR-122 knockdown enhanced cell viability and decreased cell apoptosis (P<0.05). Knockdown of miR-122 enhanced PTEN/PI3K/AKT activation and cell autophagy. Overexpression of miR-122 inhibited the PTEN/PI3K/AKT pathway and cell autophagy pathway. CONCLUSIONS The expression of miR-122 is involved in hypoxia-induced H9c2 cardiomyocyte injury. Knockdown of miR-122 protects H9c2 cells from hypoxia-induced apoptosis and enhances cell viability.

Indexed as

AnimalsApoptosisAutophagyCell HypoxiaCell MovementCells, CulturedGene Knockdown TechniquesMicroRNAsMyocardial InfarctionMyocytes, CardiacPhosphatidylinositol 3-KinaseProtective AgentsProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseRatsSignal TransductionMicroRNAsMIRN122 microRNA, ratPhosphatidylinositol 3-KinaseProtective AgentsProto-Oncogene Proteins c-aktPTEN Phosphohydrolase

Identifiers

PMID28871076
PMCPMC5597036
OpenAlexW2752320840

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.