Evidence map›Paper›PMID 32547612›Full record

ArticleJournal of geriatric cardiology : JGC2020

Ischemia/hypoxia inhibits cardiomyocyte autophagy and promotes apoptosis via the Egr-1/Bim/Beclin-1 pathway.

Bo Su, Xian-Tao Wang, Yu-Han Sun, Man-Yun Long, Jing Zheng, Wen-Hao Wu, Lang Li

Open access · greenAbstract read
In one paragraph

Article in Journal of geriatric cardiology : JGC, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

9 citing papers in PubMed, 16 citations in OpenAlex.

  1. The Role of miR-138 in Cardiovascular Diseases.BioMed research international · 2025
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  8. Mechanism of interaction between autophagy and apoptosis in cancer.Apoptosis : an international journal on programmed cell death · 2021
    Review
  9. Article
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

7 authors at 2 institutions in 1 country.

Bo SuDepartment of Cardiology, the First Affiliated Hospital of Guangxi Medical University, Nanning, China.
Xian-Tao WangDepartment of Cardiology, the First Affiliated Hospital of Guangxi Medical University, Nanning, China.
Yu-Han SunDepartment of Cardiology, the First Affiliated Hospital of Guangxi Medical University, Nanning, China.
Man-Yun LongDepartment of Cardiology, the First Affiliated Hospital of Guangxi Medical University, Nanning, China.
Jing ZhengDepartment of Cardiology, the First Affiliated Hospital of Guangxi Medical University, Nanning, China.
Wen-Hao WuDepartment of Cardiology, the First Affiliated Hospital of Guangxi Medical University, Nanning, China.
Lang LiDepartment of Cardiology, 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

backgroundMyocardial injury caused by microvascular obstruction (MVO) is characterized by persistent ischemia/hypoxia (IH) of cardiomyocytes after microembolization. Autophagy and Egr-1 were closely associated with various cardiovascular diseases, including MVO. Bim and Beclin-1 are the important genes for autophagy and apoptosis. We aimed to explore whether the Egr-1/Bim/Beclin-1 pathway is involved in regulating autophagy and apoptosis in IH-exposed cardiomyocytes.

methodsNeonatal rat cardiomyocytes exposed to the IH environment

resultsIH exposure elevated Egr-1 and Bim expressions, and decreased Beclin-1 expression in rat cardiomyocytes. Egr-1 overexpression in IH-exposed cardiomyocytes significantly up-regulated the levels of Egr-1 and Bim, and down-regulated the level of Beclin-1. Egr-1 knockdown resulted in down-regulated expressions of Egr-1 and Bim, as well as up-regulated expression of Beclin-1. In addition, Egr-1 knockdown induced autophagy was suppressed by 3-MA treatments. TEM and autophagic flux experiments also confirmed that Egr-1 inhibited autophagy progression in IH-exposed cardiomyocytes. Egr-1 suppression protected cardiomyocytes from IH-induced injury, as evidenced by the positive correlations between Egr-1 expression and LDH leakage or apoptosis index in IH-exposed cardiomyocytes.

conclusionsIH-induced cardiomyocyte autophagy and apoptosis are regulated by the Egr-1/Bim/Beclin-1 pathway, which is a potential target for treating cardiomyocyte injury caused by MVO in the IH environment.

Indexed as

ApoptosisAutophagyCardiomyocyteEgr-1Ischemia/hypoxia

Identifiers

PMID32547612
PMCPMC7276312
OpenAlexW3031070496

What OpenQuestion holds

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LicenceCC BY-NC-SA
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.