Evidence map›Paper›PMID 33179102›Full record

ArticleMolecular medicine reports2021

miR‑449a‑5p suppresses CDK6 expression to inhibit cardiomyocyte proliferation.

Bing Li, Zhi Wang, Fan Yang, Jing Huang, Xingwei Hu, Shiyan Deng, Maobo Tian, Xiaoyun Si

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

12 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. The role of microRNAs in calcific aortic valve disease.Frontiers in cardiovascular medicine · 2025
    Review
  3. Article
  4. Review
  5. MiR-449a antagonizes EMT through IL-6-mediatedMolecular therapy. Nucleic acids · 2024
    Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. 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

8 authors at 4 institutions in 1 country.

Bing LiSchool of Medicine, Guizhou University, Guiyang, Guizhou 550025, P.R. China.
Zhi WangDepartment of Emergency Medicine, Qingdao Municipal Hospital (Group), Qingdao, Shandong 266011, P.R. China.
Fan YangDepartment of Cardiology, Guizhou Provincial People's Hospital, Guiyang, Guizhou 550002, P.R. China.
Jing HuangDepartment of Cardiology, Guizhou Provincial People's Hospital, Guiyang, Guizhou 550002, P.R. China.
Xingwei HuDepartment of Cardiology, Guizhou Provincial People's Hospital, Guiyang, Guizhou 550002, P.R. China.
Shiyan DengDepartment of Cardiology, Guizhou Provincial People's Hospital, Guiyang, Guizhou 550002, P.R. China.
Maobo TianDepartment of Cardiology, Guizhou Provincial People's Hospital, Guiyang, Guizhou 550002, P.R. China.
Xiaoyun SiDepartment of Cardiology, The Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou 550004, P.R. China.
Guizhou Provincial People's Hospital · CNGuiyang Medical University · CNGuizhou University · CNQingdao University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Induction of cardiomyocyte (CM) proliferation is a promising approach for cardiac regeneration following myocardial injury. MicroRNAs (miRs) have been reported to regulate CM proliferation. In particular, miR‑449a‑5p has been identified to be associated with CM proliferation in previous high throughput functional screening data. However, whether miR‑449a‑5p regulates CM proliferation has not been thoroughly investigated. This study aimed to explore whether miR‑449a‑5p modulates CM proliferation and to identify the molecular mechanism via which miR‑449a‑5p regulates CM proliferation. The current study demonstrated that miR‑449a‑5p expression levels were significantly increased during heart development. Furthermore, the results suggested that miR‑449a‑5p mimic inhibited CM proliferation <em>in vitro</em> as determined via immunofluorescence for ki67 and histone H3 phosphorylated at serine 10 (pH3), as well as the numbers of CMs. However, miR‑449a‑5p knockdown promoted CM proliferation. CDK6 was identified as a direct target gene of miR‑449a‑5p, and CDK6 mRNA and protein expression was suppressed by miR‑449a‑5p. Moreover, CDK6 gain‑of‑function increased CM proliferation. Overexpression of CDK6 also blocked the inhibitory effect of miR‑449a‑5p on CM proliferation, indicating that CDK6 was a functional target of miR‑449a‑5p in CM proliferation. In conclusion, miR‑449a‑5p inhibited CM proliferation by targeting CDK6, which provides a potential molecular target for preventing myocardial injury.

Indexed as

3' Untranslated RegionsAnimalsCell ProliferationCells, CulturedCyclin-Dependent Kinase 6Gene Expression Regulation, DevelopmentalGene Knockdown TechniquesHeartMaleMiceMicroRNAsMyocytes, CardiacUp-Regulation3' Untranslated RegionsCdk6 protein, mouseCyclin-Dependent Kinase 6MicroRNAsMirn449 microRNA, mousecardiomyocyte proliferationCDK6microRNA‑449a‑5p

Identifiers

PMID33179102
PMCPMC7673318
OpenAlexW3096082446

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.