Evidence map›Paper›PMID 31115545›Full record

ArticleMolecular medicine reports2019

Mechanism of interactions between endoplasmic reticulum stress and autophagy in hypoxia/reoxygenation‑induced injury of H9c2 cardiomyocytes.

Gaopeng Guan, Lei Yang, Wenyin Huang, Jun Zhang, Puhua Zhang, Huan Yu, Shengyuan Liu, Xiang Gu

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

18 citing papers in PubMed, 26 citations in OpenAlex.

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  6. Pathological implications of cellular stress in cardiovascular diseases.The international journal of biochemistry & cell biology · 2023
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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

8 authors at 1 institution in 1 country.

Gaopeng GuanDepartment of Cardiology, Affiliated Hospital of Jiujiang University, Jiujiang, Jiangxi 332000, P.R. China.
Lei YangKey Laboratory of System Bio‑Medicine of Jiangxi Province, Jiujiang University, Jiujiang, Jiangxi 332000, P.R. China.
Wenyin HuangDepartment of Cardiology, Affiliated Hospital of Jiujiang University, Jiujiang, Jiangxi 332000, P.R. China.
Jun ZhangDepartment of Cardiology, Affiliated Hospital of Jiujiang University, Jiujiang, Jiangxi 332000, P.R. China.
Puhua ZhangDepartment of Cardiology, Affiliated Hospital of Jiujiang University, Jiujiang, Jiangxi 332000, P.R. China.
Huan YuKey Laboratory of System Bio‑Medicine of Jiangxi Province, Jiujiang University, Jiujiang, Jiangxi 332000, P.R. China.
Shengyuan LiuDepartment of Cardiology, Affiliated Hospital of Jiujiang University, Jiujiang, Jiangxi 332000, P.R. China.
Xiang GuDepartment of Cardiology, Affiliated Hospital of Jiujiang University, Jiujiang, Jiangxi 332000, P.R. China.
Jiujiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endoplasmic reticulum (ER) stress and autophagy are involved in myocardial ischemia‑reperfusion (I/R) injury; however, their roles in this type of injury remain unclear. The present study investigated the roles of ER stress and autophagy, and their underlying mechanisms, in H9c2 cells during hypoxia/reoxygenation (H/R) injury. Cell viability was detected by CCK‑8 assay. The autophagy flux was monitored with mCherry‑GFP‑LC3‑adenovirus transfection. The expression levels of autophagy‑related proteins and ER stress‑related proteins were measured by western blotting. Apoptosis was detected by flow cytometry and western blotting. The results indicated that autophagy was induced, ER stress was activated and apoptosis was promoted in H9c2 cells during H/R injury. The inhibition of ER stress by 4‑phenylbutyrate or C/EBP homologous protein (CHOP)‑targeting small interfering RNA (siRNA) decreased autophagy and ameliorated cell apoptosis during H/R injury. Activation of autophagy by rapamycin attenuated ER stress and ameliorated cell apoptosis. Inhibition of autophagy by 3‑methyladenine or Beclin1‑targeting siRNA aggravated ER stress and exacerbated cell apoptosis, and activation of ER stress by thapsigargin decreased autophagy and induced cell apoptosis. Collectively, the findings of the present study demonstrated that H/R induced apoptosis and autophagy via ER stress in H9c2 cells, and that CHOP may serve an important role in ER stress‑induced autophagy and apoptosis. Autophagy, as an adaptive response, was activated by ER stress and alleviated ER stress‑induced cell apoptosis during H/R injury.

Indexed as

AnimalsApoptosisAutophagyAutophagy-Related ProteinsBeclin-1Cell HypoxiaCell LineEndoplasmic Reticulum StressGene Expression RegulationHumansMyocardial Reperfusion InjuryMyocytes, CardiacPhenylbutyratesRatsRNA, Small InterferingSignal TransductionAutophagy-Related ProteinsBeclin-1Ddit3 protein, ratPhenylbutyratesRNA, Small InterferingTranscription Factor CHOP

Identifiers

PMID31115545
PMCPMC6580049
OpenAlexW2944500140

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.