Evidence map›Paper›PMID 31037501›Full record

ArticleChromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology2019

MiR-153 regulates cardiomyocyte apoptosis by targeting Nrf2/HO-1 signaling.

Xianting Zhu, Yuling Zhao, Wei Hou, Ling Guo

Abstract read
PubMed Publisher
In one paragraph

Article in Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

17 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
  2. MicroRNAs as Regulators of Radiation-Induced Oxidative Stress.Current issues in molecular biology · 2024
    Review
  3. The Role of NRF2 in Trinucleotide Repeat Expansion Disorders.Antioxidants (Basel, Switzerland) · 2024
    Review
  4. Review
  5. Interference with megalin expression/endocytic function by montelukast mitigates gentamicin nephrotoxicity: Downregulation of ClC-5 expression.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2022
    Article
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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

4 authors at 1 institution in 1 country.

Xianting ZhuDepartment of Nursing, Yidu Central Hospital of Wei Fang, No. 4138, South Linglongshan Road, Weifang, 262500, Shandong, China.
Yuling ZhaoDepartment of Emergency, Yidu Central Hospital of Wei Fang, No. 4138, South Linglongshan Road, Weifang, 262500, Shandong, China.
Wei HouDepartment of Emergency, Yidu Central Hospital of Wei Fang, No. 4138, South Linglongshan Road, Weifang, 262500, Shandong, China.
Ling GuoDepartment of Nursing, Yidu Central Hospital of Wei Fang, No. 4138, South Linglongshan Road, Weifang, 262500, Shandong, China. majiaguo1986@163.com.
Yidu Central Hospital of Weifang · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNAs (miRNAs) play various roles in the regulation of human disease, including cardiovascular diseases. MiR-153 has been previously shown to be involved in regulating neuron survival during cerebral ischemia/reperfusion (I/R) injury. However, whether miR-153 is involved in I/R-induced cardiomyocyte apoptosis remains to be elucidated. In this study, we aimed to explore the role of miR-153 in the regulation of I/R-induced cardiomyocyte apoptosis and to investigate the miR-153-mediated molecular signaling pathway responsible for its effect on cardiomyocytes using an oxygen-glucose deprivation and reoxygenation (OGD/R) cellular model. We found that OGD/R treatment induced significant upregulation of miR-153 in cardiomyocytes causing reactive oxygen species (ROS) production and cell apoptosis signaling activation and subsequently leading to cardiomyocyte apoptosis. Suppression of miR-153 protected cardiomyocytes against OGD/R treatment. We further identified that nuclear factor-like 2 (Nrf2) is a functional target of miR-153. Nrf2/ heme oxygenase-1 (HO-1) signaling plays a critical role in miR-153 regulated OGD/R-induced cardiomyocyte apoptosis. Our study indicates that the inhibition of miR-153 or restoration of Nrf2 may serve as a potential therapeutic strategy for ischemia/reperfusion injury prevention.

Indexed as

ApoptosisGlucoseHeme Oxygenase-1HumansMicroRNAsMyocardial Reperfusion InjuryMyocytes, CardiacNF-E2-Related Factor 2OxygenReactive Oxygen SpeciesSignal TransductionGlucoseHeme Oxygenase-1HMOX1 protein, humanMicroRNAsMIRN153 microRNA, humanNFE2L2 protein, humanNF-E2-Related Factor 2OxygenReactive Oxygen SpeciesApoptosisCardiomyocytesIschemia/reperfusionmiR-153Nrf2

Identifiers

PMID31037501
OpenAlexW2942699224

What OpenQuestion 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 OpenQuestion graph.