Evidence map›Paper›PMID 36172098›Full record

ArticleAnnals of translational medicine2022

MicroRNA-668-3p regulates oxidative stress and cell damage induced by Aβ1-42 by targeting the

Shengyu Li, Lishuo Wu, Meigang Ma, Longxiu Yang, Chao Qin

Open access · diamondAbstract read
In one paragraph

Article in Annals of translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.9field-weighted citation impact, top 27% 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, 11 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
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

5 authors at 2 institutions in 1 country.

Shengyu Li *Department of Neurology, Wuming Hospital of Guangxi Medical University, Nanning, China.
Lishuo Wu *Department of Neurology, The Fifth Affiliated Hospital of Guangxi Medical University, Nanning, China.
Meigang MaDepartment of Neurology, The First Affiliated Hospital of Guangxi Medical University, Nanning, China.
Longxiu YangDepartment of Neurology, The First Affiliated Hospital of Guangxi Medical University, Nanning, China.
Chao QinDepartment of Neurology, The First Affiliated Hospital of Guangxi Medical University, Nanning, China.
Guangxi Medical University · CNFirst Affiliated Hospital of GuangXi Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Alzheimer's disease (AD) is the most common type of dementia in old age and has become a serious social and medical problem threatening human health. We aimed to explore the mechanisms underlying AD development by screening for microRNAs (miRNAs) that affect AD progression and examining their role in AD development. Methods: Hematoxylin-eosin (HE) staining, immunohistochemistry, and immunofluorescence (IF) were used to analyze the characteristics of the hippocampus, neuron cell separation, and related protein expression in mice. We used Gene Expression Omnibus (GEO) data analysis to screen miRNAs and mRNAs that affect AD progression, and quantitative reverse transcription polymerase chain reaction (RT-qPCR) and western blot analysis to determine changes in miRNA and mRNA levels before and after amyloid β (Aβ)1-42 induction. In addition, we used luciferase analysis to examine miRNA and mRNA binding and the effect of miRNA/mRNA interaction on neuronal cell proliferation. Apoptosis and reactive oxygen species (ROS) levels were examined using Cell Counting Kit-8 analysis and flow cytometry (FCM), respectively. The enzyme-linked immunosorbent assay was used to analyze changes in neuronal cell-secreted oxidative stress-related protein levels through miRNA/mRNA interaction. Results: Oxidative stress levels were significantly increased in the AD mouse model. GEO data analysis revealed 67 dysregulated miRNAs, and miR-668-3p was identified as a potential therapeutic target for AD. We found that the AD and Aβ1-42-induced models showed an increase in miR-668-3p and a decrease in oxidation resistance 1 ( Conclusions: MiR-668-3p negatively regulated

Indexed as

Alzheimer’s disease (AD)miR-668-3pOXR1p21p53

Identifiers

PMID36172098
PMCPMC9511202
OpenAlexW4294693732

What Socratic 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 Socratic graph.