Evidence map›Paper›PMID 35692592›Full record

ArticleBioMed research international2022

miR-211-5p Alleviates the Myocardial Ischemia Injury Induced by Ischemic Reperfusion Treatment via Targeting FBXW7.

Yonghui Liu, Jiatian Meng, Hongqin Di, Liheng Zheng, Zili Meng

RetractedOpen access · hybridAbstract readRetracted Publication
In one paragraph

Article in BioMed research international, 2022. 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 It has been retracted, and should not be counted.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 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.3field-weighted citation impact, top 45% 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

2 citing papers in PubMed, 2 citations in OpenAlex.

  1. Article
  2. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Yonghui LiuDepartment of Cardiovascular Surgery, Hebei Chest Hospital, Hebei Lung Cancer Research Center, Shijiazhuang, 050041 Hebei, China.
Jiatian MengDepartment of Radiology, Hebei Chest Hospital, Hebei Lung Cancer Research Center, Shijiazhuang, 050041 Hebei, China.
Hongqin DiMolecular Biology Laboratory, Hebei Chest Hospital, Hebei Lung Cancer Research Center, Shijiazhuang, 050041 Hebei, China.
Liheng ZhengDepartment of Laboratory, Hebei Chest Hospital, Hebei Lung Cancer Research Center, Shijiazhuang, 050041 Hebei, China.
Zili MengDepartment of Cardiovascular Surgery, Hebei Chest Hospital, Hebei Lung Cancer Research Center, Shijiazhuang, 050041 Hebei, China.ORCID https://orcid.org/0000-0001-5720-9559
Hospital of Hebei Province · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiovascular diseases, a class of the most common diseases, seriously threaten human health, which is a direct inducement of death in most countries. The restoration of blood supply is an impactful intervention way for cardiovascular disease treatments while the injury induced by oxygen-glucose deprivation and ischemic reperfusion (I/R) may further impact the tissues of the patients. Myocardial reperfusion is a precondition for saving ischemic myocardial tissues in acute myocardial infarction while the injury induced by immediate reperfusion takes a great challenge for cardiovascular disease treatment. Howbeit, the reperfusion of coronary blood could aggravate the injury triggered by ischemia. At present, several studies have focused on the etiopathogenesis and therapeutic strategies of ischemia-reperfusion injury of the myocardium. The report has verified that miR-211-5p was elevated in the pathological specimens, while the influence of miR-211-5p in I/R-mediated injury of myocardial cells remains unclear. This research is aimed at illustrating the role of miR-211-5p in the progression of I/R injury of myocardial cells, and qRT-PCR, western blot, CCK-8, and TUNEL assay were used to investigate the functions of miR-211-5p on I/R-mediated injury of myocardial cells. The result mirrored that miR-211-5p was distinctly reduced in the I/R-induced AC16, and reduced miR-211-5p could evidently improve the viability of I/R-induced AC16. miR-211-5p could directly target FBXW7, and FBXW7 upregulation could reverse the improvement of AC16 in viability and apoptosis level after suffering I/R. Moreover, it was also proved that miR-211-5p can mediate the activation of Wnt/

Indexed as

MicroRNAsMyocardial InfarctionMyocardial IschemiaMyocardial Reperfusion InjuryReperfusion InjuryApoptosisF-Box-WD Repeat-Containing Protein 7HumansMyocytes, CardiacReperfusionF-Box-WD Repeat-Containing Protein 7FBXW7 protein, humanMicroRNAsMIRN211 microRNA, human

Identifiers

PMID35692592
PMCPMC9187464
OpenAlexW4281679224

What OpenQuestion holds

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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 OpenQuestion graph.