Evidence map›Paper›PMID 30604587›Full record

ArticleJournal of cellular and molecular medicine2019

MiR-103 inhibiting cardiac hypertrophy through inactivation of myocardial cell autophagy via targeting TRPV3 channel in rat hearts.

Hanping Qi, Jing Ren, Mingyao E, Qianhui Zhang, Yonggang Cao, Lina Ba, Chao Song, Pilong Shi, Bowen Fu, Hongli Sun

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 15% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.

  1. Pooled it
  2. Role of miR-155 and miR-103 in Oxidative Stress in Cardiovascular Disease: A Narrative Review.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026
    Review
  3. Empagliflozin modulates microRNA expression in human primary cardiomyocytes under CoClInternational journal of cardiology. Cardiovascular risk and prevention · 2026
    Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. TRPV3: Structure, Diseases and Modulators.Molecules (Basel, Switzerland) · 2023
    Review
  10. Long noncoding RNAOpen medicine (Warsaw, Poland) · 2023
    Article
  11. Article
  12. Neutrophil-like cell membrane-coated siRNA of lncRNAMolecular therapy. Nucleic acids · 2022
    Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. MicroRNA-369 attenuates hypoxia-induced cardiomyocyte apoptosis and inflammation via targeting TRPV3.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2021
    Article
  19. Article
  20. 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

10 authors at 1 institution in 1 country.

Hanping QiDepartment of Pharmacology, Harbin Medical University-Daqing, Daqing, China.
Jing RenDepartment of Pharmacology, Harbin Medical University-Daqing, Daqing, China.
Mingyao EDepartment of Pharmacology, Harbin Medical University-Daqing, Daqing, China.
Qianhui ZhangDepartment of Pharmacology, Harbin Medical University-Daqing, Daqing, China.
Yonggang CaoDepartment of Pharmacology, Harbin Medical University-Daqing, Daqing, China.
Lina BaDepartment of Pharmacology, Harbin Medical University-Daqing, Daqing, China.
Chao SongDepartment of Pharmacology, Harbin Medical University-Daqing, Daqing, China.
Pilong ShiDepartment of Pharmacology, Harbin Medical University-Daqing, Daqing, China.
Bowen FuDepartment of Pharmacology, Harbin Medical University-Daqing, Daqing, China.
Hongli SunDepartment of Pharmacology, Harbin Medical University-Daqing, Daqing, China.ORCID 0000-0002-6495-6103
Harbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiac hypertrophy is a common pathological change frequently accompanied by chronic hypertension and myocardial infarction. Nevertheless, the pathophysiological mechanisms of cardiac hypertrophy have never been elucidated. Recent studies indicated that miR-103 expression was significantly decreased in heart failure patients. However, less is known about the role of miR-103 in cardiac hypertrophy. The present study was designed to investigate the relationship between miR-103 and the mechanism of pressure overload-induced cardiac hypertrophy. TRPV3 protein, cardiac hypertrophy marker proteins (BNP and β-MHC) and autophagy associated proteins (Beclin-1 and LC3-II) were up-regulated, as well as, miR-103 expression and autophagy associated proteins (p62) were down-regulated in cardiac hypertrophy models in vivo and in vitro respectively. Further results indicated that silencing TRPV3 or forcing overexpression of miR-103 could dramatically inhibit cell surface area, relative fluorescence intensity of Ca

Indexed as

Angiotensin IIAnimalsAutophagyBeclin-1CardiomegalyCells, CulturedDown-RegulationHeartHeart FailureMaleMicroRNAsMyocytes, CardiacRatsRats, WistarSignal TransductionTRPV Cation ChannelsAngiotensin IIBeclin-1MicroRNAsMIRN103 microRNA, ratTRPV3 protein, ratTRPV Cation Channelsautophagycardiac hypertrophymiR-103TRPV3

Identifiers

PMID30604587
PMCPMC6378213
OpenAlexW2907688633

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.