Evidence map›Paper›PMID 30507047›Full record

ArticleCell proliferation2019

Role of miR-223-3p in pulmonary arterial hypertension via targeting ITGB3 in the ECM pathway.

Aijun Liu, Yifan Liu, Bin Li, Ming Yang, Yang Liu, Junwu Su

Open access · hybridAbstract read
In one paragraph

Article in Cell proliferation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

33 citing papers in PubMed, 52 citations in OpenAlex.

  1. Review
  2. The emerging role of integrin signaling in pulmonary vascular disease.American journal of physiology. Lung cellular and molecular physiology · 2026
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Targeting integrin pathways: mechanisms and advances in therapy.Signal transduction and targeted therapy · 2023
    Review
  12. Review
  13. Review
  14. Article
  15. Review
  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

6 authors at 1 institution in 1 country.

Aijun LiuDepartment of Pediatric Cardiac Surgery Center, Beijing Anzhen Hospital, Capital Medical University, Beijing, China.
Yifan LiuWeifang Medicial University, Weifang, China.
Bin LiDepartment of Pediatric Cardiac Surgery Center, Beijing Anzhen Hospital, Capital Medical University, Beijing, China.
Ming YangDepartment of Pediatric Cardiac Surgery Center, Beijing Anzhen Hospital, Capital Medical University, Beijing, China.
Yang LiuDepartment of Pediatric Cardiac Surgery Center, Beijing Anzhen Hospital, Capital Medical University, Beijing, China.
Junwu SuDepartment of Pediatric Cardiac Surgery Center, Beijing Anzhen Hospital, Capital Medical University, Beijing, China.ORCID http://orcid.org/0000-0001-7378-2515
Capital Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesTo investigate the functions of miR-223-3p and ITGB3 in pulmonary arterial hypertension (PAH). MATERIALS AND

methodsMicroarray analysis was used to detect differentially expressed genes and microRNAs. In in vitro models, the expressions of miR-223-3p and ITGB3 were detected by qRT-PCR and Western blot. α-SMA expression and cell proliferation were analysed by immunofluorescence and MTT assay, respectively. In in vivo models, PAH progressions were determined by measuring the levels of mPAP and RVSP. Lung and myocardial tissues were subjected to HE staining and Masson and Sirius red-saturated carbazotic acid staining to investigate the pathological features.

resultsThe microarray analysis revealed that ITGB3 was upregulated, while hsa-miR-223-3p was downregulated in PAH. After the induction of hypoxia, miR-223-3p was downregulated and ITGB3 was upregulated in PASMCs. Hypoxia induction promoted cell proliferation and inhibited α-SMA expression in PASMCs. Both the upregulation of miR-223-3p and the downregulation of ITGB3 attenuated the aberrant proliferation induced by hypoxia conditions. After approximately 4 weeks, the mPAP and RVSP levels of rats injected with MCT were decreased by the overexpression of miR-223-3p or the silencing of ITGB3. The staining results revealed that both miR-223-3p overexpression and ITGB3 knockdown alleviated the pulmonary vascular remodelling and improved the PAH pathological features of rats.

conclusionsMiR-223-3p alleviated the progression of PAH by suppressing the expression of ITGB3, a finding which provides novel targets for clinical treatment.

Indexed as

Down-RegulationUp-RegulationAnimalsApoptosisCell HypoxiaCell ProliferationCells, CulturedFamilial Primary Pulmonary HypertensionIntegrin beta3MaleMicroRNAsRats, Sprague-DawleyIntegrin beta3MicroRNAsMIRN223 microRNA, ratITGB3MiR-223-3ppulmonary arterial smooth muscle cellpulmonary hypertension

Identifiers

PMID30507047
PMCPMC6496671
OpenAlexW2902131197

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.