Evidence map›Paper›PMID 35899226›Full record

ArticleEvidence-based complementary and alternative medicine : eCAM2022

miR-214-3p Protects and Restores the Myocardial Tissue of Rat Myocardial Infarction Model by Targeting PTEN.

Yuan Cheng, Qing He, Tao Jin, Na Li

RetractedOpen access · hybridAbstract readRetracted Publication
In one paragraph

Article in Evidence-based complementary and alternative medicine : eCAM, 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 It has been retracted, and should not be counted.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 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 43% 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

4 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Review
  3. Oxidative medicine and cellular longevity · 2023
    Article
  4. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Yuan ChengKey Laboratory of Advanced Technologies of Materials, Ministry of Education, Southwest Jiaotong University, Chengdu 610031, China.
Qing HeKey Laboratory of Advanced Technologies of Materials, Ministry of Education, Southwest Jiaotong University, Chengdu 610031, China.ORCID https://orcid.org/0000-0003-4928-4609
Tao JinKey Laboratory of Advanced Technologies of Materials, Ministry of Education, Southwest Jiaotong University, Chengdu 610031, China.
Na LiKey Laboratory of Advanced Technologies of Materials, Ministry of Education, Southwest Jiaotong University, Chengdu 610031, China.
Southwest Jiaotong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myocardial infarction (MI), which results in myocardial cell dysfunction and irreversible loss, is one of the most serious health threats today. This study was started with rats, by which the consequence of miRNA expression dysregulation to the occurrence and progression of cardiovascular diseases was explored. We first conducted miRNA sequencing on the myocardial tissues separately from myocardial infarction treatment and sham operation treatment to clarify those differently expressed miRNAs; then, our experiment of functional verification of those key miRNAs was initiated so as to dig out the molecular mechanism behind the miRNA's regulation in myocardial infarction. And it turned out that there were 32 upregulated miRNAs and 16 downregulated miRNAs according to our comparison from the myocardial infarction model group to the sham operation group; of all those upregulated, alteration in miR-214-3p expression was the most conspicuous. Overexpression of miR-214-3p greatly alleviated myocardial infarct area and ameliorated myocardial tissue structure, even reducing myocardial fibrosis and the devastation in the tissues. On the molecular level, miR-214-3p overexpression brought down both the apoptosis rate and cleaved caspase 3 expression. Besides that, we verified that PTEN is the target gene of miR-214-3p through a dual-luciferase assay. A cotransfection of miR-214-3p and PTEN brought about an obvious elevation in the myocardial infarct area, tissue damage, and fibrosis, even in the aspect of cellular apoptosis than a mere transfection of miR-214-3p. All the results above verified miR-214-3p's effects in protecting myocardial tissues and reducing the infarct area, and it was reasonable to assume that those functions of miR-214-3p came into effect by targeting PTEN, which was then justified by the inversion to miR-214-3p's protection via PTEN overexpression.

Identifiers

PMID35899226
PMCPMC9313954
OpenAlexW4285729977

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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.