Evidence map›Paper›PMID 28415624›Full record

ArticleOncotarget2017

Hypoxia-inducible factor 1a induces phenotype switch of human aortic vascular smooth muscle cell through PI3K/AKT/AEG-1 signaling.

Kai Liu, Changcun Fang, Yuwen Shen, Zhengqin Liu, Min Zhang, Bingbing Ma, Xinyan Pang

RetractedOpen access · diamondAbstract readRetracted Publication
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

27 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
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  5. Review
  6. Article
  7. Reoxygenation Modulates the Adverse Effects of Hypoxia on Wound Repair.International journal of molecular sciences · 2022
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  17. Article
  18. Photo-functionalized TiOBioactive materials · 2021
    Article
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  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Kai LiuDepartment of Cardiovascular Surgery, Qilu Hospital of Shandong University, Jinan 250012, Shandong, China.
Changcun FangDepartment of Cardiovascular Surgery, Qilu Hospital of Shandong University, Jinan 250012, Shandong, China.
Yuwen ShenDepartment of Cardiovascular Surgery, Qilu Hospital of Shandong University, Jinan 250012, Shandong, China.
Zhengqin LiuDepartment of Cardiovascular Surgery, Qilu Hospital of Shandong University, Jinan 250012, Shandong, China.
Min ZhangDepartment of Cardiovascular Surgery, Qilu Hospital of Shandong University, Jinan 250012, Shandong, China.
Bingbing MaDepartment of Cardiovascular Surgery, Qilu Hospital of Shandong University, Jinan 250012, Shandong, China.
Xinyan PangDepartment of Cardiovascular Surgery, Qilu Hospital of Shandong University, Jinan 250012, Shandong, China.
Qilu Hospital of Shandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To date, hypoxia-inducible factor 1a (HIF-1a) and astrocyte elevated gene-1 (AEG-1) have been involved in the proliferation, migration and morphological changes of vascular smooth muscle cells. However, the potential relationship of HIF-1a-AEG-1 pathway in human aortic smooth muscle cell (HASMC) has not been reported. In the present study, in-vitro assays were utilized to explore the potential impact of HIF-1a-AEG-1 signaling on HASMC phenotype. Here, we found that HIF-1a expression was up-regulated in the media of thoracic aortic dissection tissues as compared with normal aortic tissues, and was associated with increased apoptotic SMCs and decreased AEG-1 expression. Mechanically, hypoxia promoted the expression of HIF-1a by PI3K-AKT pathway in HASMCs; HIF-1a further suppressed the expressions of AEG-1, a-SMA and SM22a, and promoted osteopontin (OPN) expression. Functionally, HIF-1a inhibited the proliferation and migration of HASMCs. However, si-HIF-1a or Akt inhibitor abrogated HIF-1a-mediated related expressions and biological effects above. In conclusion, HIF-1a induces HASMC phenotype switch, and closely related to PI3K/AKT and AEG-1 signaling, which may provide new avenues for the prevention and treatment of aortic dissection diseases.

Indexed as

AortaAortic DissectionApoptosisBiomarkersCell Adhesion MoleculesCell MovementCell ProliferationCells, CulturedGene ExpressionHumansHypoxiaHypoxia-Inducible Factor 1, alpha SubunitMembrane ProteinsMuscle, Smooth, VascularMyocytes, Smooth MusclePhenotypeBiomarkersCell Adhesion MoleculesHypoxia-Inducible Factor 1, alpha SubunitMembrane ProteinsMTDH protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRNA-Binding ProteinsHASMCHIF-1aPI3K/AKT/AEG-1

Identifiers

PMID28415624
PMCPMC5464872
OpenAlexW2598652858

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.