Evidence map›Paper›PMID 31802847›Full record

ArticleDrug design, development and therapy2019

MicroRNA-384-5p/Beclin-1 As Potential Indicators For Epigallocatechin Gallate Against Cardiomyocytes Ischemia Reperfusion Injury By Inhibiting Autophagy Via PI3K/Akt Pathway.

Chan Zhang, Ronggan Liang, Xiaowen Gan, Xiufang Yang, LingLin Chen, Jie Jian

Open access · goldAbstract read
In one paragraph

Article in Drug design, development and therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
4.0field-weighted citation impact, top 6% 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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.

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  11. Structural Color Colloidal Photonic Crystals for Biomedical Applications.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
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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

6 authors at 2 institutions in 1 country.

Chan ZhangDepartment of Pharmacology, Xiangya Hospital, Central South University, Changsha, Hunan, People's Republic of China.
Ronggan LiangDepartment of Pharmacology, Guilin Medical University, Guilin, Guangxi, People's Republic of China.
Xiaowen GanDepartment of Pharmacology, Guilin Medical University, Guilin, Guangxi, People's Republic of China.
Xiufang YangDepartment of Pharmacology, Guilin Medical University, Guilin, Guangxi, People's Republic of China.
LingLin ChenDepartment of Pharmacology, Guilin Medical University, Guilin, Guangxi, People's Republic of China.
Jie JianDepartment of Pharmacology, Guilin Medical University, Guilin, Guangxi, People's Republic of China.ORCID 0000-0003-0569-1149
Guilin Medical University · CNCentral South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

aimsEpigallocatechin gallate (EGCG) has established protective actions against myocardial ischemia/reperfusion (I/R) injury by regulating autophagy. However, little is known about the mechanisms of EGCG in posttranscriptional regulation in the process of cardioprotection. Here we studied whether microRNAs play a role in EGCG-induced cardioprotection.

methodsThe myocardial I/R injury in vitro and in vivo model were made, with or without EGCG pretreatment. The upregulation and silencing of microRNA-384-5p (miR-384) and Beclin-1 in H9c2 cell lines were established. Rats were transfected with miR-384 specific shRNA. Dual-luciferase reporter gene assay was conducted to verify the relationship between miR-384 and Beclin-1. TTC staining was performed to analyze the area of myocardial infarct size. Cell viability was monitored by cell counting kit-8 (CCK-8). The release of cardiac troponin-I (cTnI) was examined by ELISA. The levels of autophagy-related genes or proteins expression were evaluated by qRT-PCR or Western blotting. Autophagosomes of myocardial cells were detected by transmission electron microscopy and laser scanning confocal microscope.

resultsI/R increased both autophagosomes and autolysosomes, thereby increasing autophagic flux both in vitro and in vivo. Pretreatment with EGCG attenuated I/R-induced autophagic flux expression, accompanied by an increase in cell viability and a decrease in the size of myocardial infarction. MiR-384 expression was down-regulated in H9c2 cell lines when subjected to I/R, while this suppression could be reversed by EGCG pretreatment. The dual-luciferase assay verified that Beclin-1 was a target of miR-384. Both overexpression of miR-384 and knocking down of Beclin-1 significantly inhibited I/R-induced autophagy, accompanied by the activation of PI3K/Akt pathway, thus enhanced the protective effect of EGCG. However, these functions were abrogated by the PI3K inhibitor, LY294002.

conclusionWe confirmed that EGCG has a protective role in microRNA-384-mediated autophagy by targeting Beclin-1 via activating the PI3K/Akt signaling pathway. Our results unveiled a novel role of EGCG in myocardial protection, involving posttranscriptional regulation with miRNA-384.

Indexed as

AnimalsAutophagyBeclin-1CatechinCells, CulturedCell SurvivalDisease Models, AnimalDose-Response Relationship, DrugHEK293 CellsHumansMicroRNAsMolecular StructureMyocardial Reperfusion InjuryNeuroprotective AgentsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktBeclin-1Catechinepigallocatechin gallateMicroRNAsMIRN384 microRNA, ratNeuroprotective AgentsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktautophagyBeclin-1epigallocatechin gallateischemia/reperfusionmicroRNA-384-5pPI3K/Akt pathway

Identifiers

PMID31802847
PMCPMC6802542
OpenAlexW2980793704

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.