Evidence map›Paper›PMID 19336275›Full record

ArticleJournal of molecular and cellular cardiology2009

MicroRNA-21 protects against the H(2)O(2)-induced injury on cardiac myocytes via its target gene PDCD4.

Yunhui Cheng, Xiaojun Liu, Shuo Zhang, Ying Lin, Jian Yang, Chunxiang Zhang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of molecular and cellular cardiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 196 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
196citing papers in PubMed, 3 pooled it
10.8field-weighted citation impact, top 1% 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

196 citing papers in PubMed, 3 syntheses or guidelines pooled it, 365 citations in OpenAlex.

  1. Pooled it
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  4. Trial
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  6. Review
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  14. Article
  15. Observational
  16. The interplay of hydrogen sulfide and microRNAs in cardiovascular diseases: insights and future perspectives.Mammalian genome : official journal of the International Mammalian Genome Society · 2024
    Review
  17. Review
  18. Article
  19. miRNAs in Heart Development and Disease.International journal of molecular sciences · 2024
    Review
  20. Article

136 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Yunhui ChengRNA and Cardiovascular Research Laboratory, Department of Anesthesiology, New Jersey Medical School, University of Medicine and Dentistry of New Jersey, Newark, NJ 07101-1709, USA.
Xiaojun Liu
Shuo Zhang
Ying Lin
Jian Yang
Chunxiang Zhang
Rutgers New Jersey Medical SchoolUniversity Hospital, Newark · US

Funding

Role of miR-145 in Vascular Smooth Muscle Cell BiologyRole ofR01HL095707 · NHLBI · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI ZHANG, CHUNXIANG · 2010 to 2013
$1.5M
MPO and NO signaling in neointima formationR01HL080133 · NHLBI · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI ZHANG, CHUNXIANG · 2006 to 2010
$1.5M
NHLBI NIH HHS HL080133NHLBI NIH HHS R01 HL080133NHLBI NIH HHS R01 HL095707
6 · The paper itself

Abstract

Reactive oxygen species (ROS)-induced cardiac cell injury via expression changes of multiple genes plays a critical role in the pathogenesis of numerous heart diseases. MicroRNAs (miRNAs) comprise a novel class of endogenous, small, noncoding RNAs that negatively regulate about 30% of the genes in a cell via degradation or translational inhibition of their target mRNAs. Currently, the effects of ROS on miRNA expression and the roles of miRNAs in ROS-mediated injury on cardiac myocytes are uncertain. Using quantitative real-time RT-PCR (qRT-PCR), we demonstrated that microRNA-21 (miR-21) was upregulated in cardiac myocytes after treatment with hydrogen peroxide (H(2)O(2)). To determine the potential roles of miRNAs in H(2)O(2)-mediated gene regulation and cellular injury, miR-21 expression was downregulated by miR-21 inhibitor and upregulated by pre-miR-21. H(2)O(2)-induced cardiac cell death and apoptosis were increased by miR-21 inhibitor and was decreased by pre-miR-21. Programmed cell death 4 (PDCD4) that was regulated by miR-21 and was a direct target of miR-21 in cardiac myocytes. Pre-miR-21-mediated protective effect on cardiac myocyte injury was inhibited in H(2)O(2)-treated cardiac cells via adenovirus-mediated overexpression of PDCD4 without miR-21 binding site. Moreover, Activator protein 1 (AP-1) was a downstream signaling molecule of PDCD4 that was involved in miR-21-mediated effect on cardiac myocytes. The results suggest that miR-21 is sensitive to H(2)O(2) stimulation. miR-21 participates in H(2)O(2)-mediated gene regulation and functional modulation in cardiac myocytes. miR-21 might play an essential role in heart diseases related to ROS such as cardiac hypertrophy, heart failure, myocardial infarction, and myocardial ischemia/reperfusion injury.

Indexed as

AnimalsApoptosisApoptosis Regulatory ProteinsBlotting, WesternHydrogen PeroxideMicroRNAsMyocytes, CardiacNecrosisRatsRats, Sprague-DawleyReverse Transcriptase Polymerase Chain ReactionTranscription Factor AP-1Apoptosis Regulatory ProteinsHydrogen PeroxideMicroRNAsmirn21 microRNA, ratPdcd4 protein, ratTranscription Factor AP-1

Identifiers

PMID19336275
PMCPMC3593965
OpenAlexW2141570739

What OpenQuestion holds

Textmetadata
LicenceTDM
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.