Evidence map›Paper›PMID 31444671›Full record

ArticleIn vitro cellular & developmental biology. Animal2019

Protective effect of miR-20a against hypoxia/reoxygenation treatment on cardiomyocytes cell viability and cell apoptosis by targeting TLR4 and inhibiting p38 MAPK/JNK signaling.

Xin-Yu Gong, Yun Zhang

Abstract read
PubMed Publisher
In one paragraph

Article in In vitro cellular & developmental biology. Animal, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.8field-weighted citation impact, top 34% 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

11 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Expression Analysis ofInternational journal of molecular and cellular medicine · 2025
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  5. Review
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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

2 authors at 1 institution in 1 country.

Xin-Yu GongInternational Medical Department, China-Japan Friendship Hospital, Beijing, 100029, People's Republic of China. gongxinyu0001@163.com.
Yun ZhangInternational Medical Department, China-Japan Friendship Hospital, Beijing, 100029, People's Republic of China.
China-Japan Friendship Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNAs (miRNAs) are recognized to hold essential parts in the course of pathophysiology participating in myocardial ischemia/reperfusion (I/R) injury. The current study was intended to appraise the functional implication and underlying regulatory mechanism action of miR-20a in myocardial I/R injury. In cardiomyocyte hypoxia/reoxygenation (H/R) model simulating I/R, we observed that miR-20a was diminished in H9c2 cells subjected to H/R. The miR-20a mimics promoted cardiomyocyte viability and reduced H/R-triggered cell apoptosis, while the miR-20a inhibitors induced the inverse response in H9c2 cells subjected to H/R injury. Moreover, we ascertained that TLR4 was one downstream target gene of miR-20a and revealed that miR-20a might hold its protective action on cardiomyocytes subjected to H/R by inactivating p38 MAPK/JNK signaling. In summary, this study highlighted the relieved potential of miR-20a against cardiomyocyte H/R injury and suggested its favorable therapeutic role for myocardial I/R injury.

Indexed as

AnimalsApoptosisCell HypoxiaCell LineCell SurvivalGene Expression RegulationMAP Kinase Kinase 4MicroRNAsMyocardial Reperfusion InjuryMyocytes, CardiacOxygenp38 Mitogen-Activated Protein KinasesRatsSignal TransductionToll-Like Receptor 4MAP Kinase Kinase 4MicroRNAsMIRN20 microRNA, ratOxygenp38 Mitogen-Activated Protein KinasesTlr4 protein, ratToll-Like Receptor 4miR-20aMyocardial I/R injuryp38 MAPK/JNK pathwayTLR4

Identifiers

PMID31444671
OpenAlexW2969668461

What Socratic holds

Textmetadata
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.