Evidence map›Paper›PMID 29207010›Full record

ArticleInternational journal of molecular medicine2018

The potential inhibitory effects of miR‑19b on vulnerable plaque formation via the suppression of STAT3 transcriptional activity.

Sufang Li, Qiang Geng, Hong Chen, Jing Zhang, Chengfu Cao, Feng Zhang, Junxian Song, Chuanfen Liu, Wenqing Liang

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
0.8field-weighted citation impact, top 31% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
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  5. Review
  6. Review
  7. Molecular basis of acute coronary syndrome.Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences · 2022
    Review
  8. Article
  9. Therapeutic Value of miRNAs in Coronary Artery Disease.Oxidative medicine and cellular longevity · 2021
    Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. 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

9 authors at 3 institutions in 1 country.

Sufang LiDepartment of Cardiology, Peking University People's Hospital, Beijing 100044, P.R. China.
Qiang GengDepartment of Cardiology, Qingdao Municipal Hospital, Qingdao, Shandong 266011, P.R. China.
Hong ChenDepartment of Cardiology, Peking University People's Hospital, Beijing 100044, P.R. China.
Jing ZhangDepartment of Cardiology, Peking University People's Hospital, Beijing 100044, P.R. China.
Chengfu CaoDepartment of Cardiology, Peking University People's Hospital, Beijing 100044, P.R. China.
Feng ZhangDepartment of Cardiology, Peking University People's Hospital, Beijing 100044, P.R. China.
Junxian SongDepartment of Cardiology, Peking University People's Hospital, Beijing 100044, P.R. China.
Chuanfen LiuDepartment of Cardiology, Peking University People's Hospital, Beijing 100044, P.R. China.
Wenqing LiangDepartment of Cardiology, Peking University People's Hospital, Beijing 100044, P.R. China.
Peking University People's Hospital · CNPeking University · CNQingdao Municipal Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atherosclerotic plaque growth requires angiogenesis, and acute coronary syndrome (ACS) is usually triggered by the rupture of unstable atherosclerotic plaques. Previous studies have identified typically circulating microRNA (miRNA/miR) profiles in patients with ACS. miRNAs serve important roles in the pathophysiology of atherosclerotic plaque progression. The present study aimed to investigate the potential role and mechanism of miR‑19b in plaque stability. miRNA array data indicated that 28 miRNAs were differentially expressed in the plasma of patients with unstable angina (UA; n=12) compared with in control individuals (n=12), and miR‑19b exhibited the most marked upregulation. Circulating miR‑19b levels were further validated in another independent cohort, which consisted of 34 patients with UA and 24 controls, by quantitative polymerase chain reaction. Gene Ontology annotations of the predicted target genes of miR‑19b suggested that miR‑19b may be involved in endothelial cell (EC) proliferation, migration and angiogenesis, which was confirmed by Cell Counting kit‑8, wound healing and tube formation assays in the present study. Finally, the present study indicated that miR‑19b may suppress signal transducer and activator of transcription 3 (STAT3) tyrosine phosphorylation and transcriptional activity in ECs, as determined by western blot analysis and luciferase reporter assay. In conclusion, the present study revealed that increased miR‑19b expression may delay unstable plaque progression in patients with UA by inhibiting EC proliferation, migration and angiogenesis via the suppression of STAT3 transcriptional activity.

Indexed as

AtherosclerosisCell Culture TechniquesCell ProliferationEndothelial CellsFemaleGene Expression RegulationHumansMaleMicroRNAsMiddle AgedNeovascularization, PathologicPlaque, AtheroscleroticSignal TransductionSTAT3 Transcription FactorMicroRNAsSTAT3 protein, humanSTAT3 Transcription Factor

Identifiers

PMID29207010
PMCPMC5752162
OpenAlexW2768315850

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.