Evidence map›Paper›PMID 25898913›Full record

ArticleJournal of cellular and molecular medicine2015

MicroRNA-181c targets Bcl-2 and regulates mitochondrial morphology in myocardial cells.

Hongjiang Wang, Jing Li, Hongjie Chi, Fan Zhang, Xiaoming Zhu, Jun Cai, Xinchun Yang

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

37 citing papers in PubMed, 53 citations in OpenAlex.

  1. Article
  2. Review
  3. Epigenetic Mechanisms in Heart Diseases.Reviews in cardiovascular medicine · 2025
    Review
  4. Article
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  7. Article
  8. Article
  9. Article
  10. The Role of MicroRNAs in Mitochondria-Mediated Eye Diseases.Frontiers in cell and developmental biology · 2021
    Review
  11. Article
  12. Article
  13. Article
  14. Cells · 2020
    Review
  15. Article
  16. Review
  17. Review
  18. 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

7 authors at 1 institution in 1 country.

Hongjiang WangDepartment of Cardiology, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China.
Jing LiDepartment of Cardiology, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China.
Hongjie ChiDepartment of Cardiology, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China.
Fan ZhangDepartment of Cardiology, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China.
Xiaoming ZhuDepartment of Cardiology, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China.
Jun CaiDepartment of Cardiology, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China.
Xinchun YangDepartment of Cardiology, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China.
Capital Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Apoptosis is an important mechanism for the development of heart failure. Mitochondria are central to the execution of apoptosis in the intrinsic pathway. The main regulator of mitochondrial pathway of apoptosis is Bcl-2 family which includes pro- and anti-apoptotic proteins. MicroRNAs are small noncoding RNA molecules that regulate gene expression by inhibiting mRNA translation and/or inducing mRNA degradation. It has been proposed that microRNAs play critical roles in the cardiovascular physiology and pathogenesis of cardiovascular diseases. Our previous study has found that microRNA-181c, a miRNA expressed in the myocardial cells, plays an important role in the development of heart failure. With bioinformatics analysis, we predicted that miR-181c could target the 3' untranslated region of Bcl-2, one of the anti-apoptotic members of the Bcl-2 family. Thus, we have suggested that miR-181c was involved in regulation of Bcl-2. In this study, we investigated this hypothesis using the Dual-Luciferase Reporter Assay System. Cultured myocardial cells were transfected with the mimic or inhibitor of miR-181c. We found that the level of miR-181c was inversely correlated with the Bcl-2 protein level and that transfection of myocardial cells with the mimic or inhibitor of miR-181c resulted in significant changes in the levels of caspases, Bcl-2 and cytochrome C in these cells. The increased level of Bcl-2 caused by the decrease in miR-181c protected mitochondrial morphology from the tumour necrosis factor alpha-induced apoptosis.

Indexed as

3' Untranslated RegionsAnimalsApoptosisBase SequenceBlotting, WesternCell SurvivalConserved SequenceDNA, MitochondrialGene Expression RegulationGenes, ReporterGreen Fluorescent ProteinsMiceMicroRNAsMitochondria, HeartMitochondrial MembranesMolecular Sequence Data3' Untranslated RegionsDNA, Mitochondrialenhanced green fluorescent proteinGreen Fluorescent ProteinsMicroRNAsmirn181 microRNA, mouseProto-Oncogene Proteins c-bcl-2Tumor Necrosis Factor-alphaapoptosisbcl-2microRNAmitochondria

Identifiers

PMID25898913
PMCPMC4568913
OpenAlexW2007220581

What OpenQuestion holds

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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.