Evidence map›Paper›PMID 27363580›Full record

ArticleScientific reports2016

Inhibition of hypoxia inducible factor-1α attenuates abdominal aortic aneurysm progression through the down-regulation of matrix metalloproteinases.

Shih-Hung Tsai, Po-Hsun Huang, Yu-Juei Hsu, Yi-Jen Peng, Chien-Hsing Lee, Jen-Chun Wang, Jaw-Wen Chen, Shing-Jong Lin

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
8.5field-weighted citation impact, top 2% 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

51 citing papers in PubMed, 88 citations in OpenAlex.

  1. Article
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  14. NADPH Oxidases in Aortic Aneurysms.Antioxidants (Basel, Switzerland) · 2022
    Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  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

8 authors at 4 institutions in 1 country.

Shih-Hung TsaiDepartment of Emergency Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan.
Po-Hsun HuangInstitute of Clinical Medicine, National Yang-Ming University, Taipei, Taiwan.
Yu-Juei HsuDivision of Nephrology, Department of medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan.
Yi-Jen PengDepartment of Pathology, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan.
Chien-Hsing LeeDivision of Endocrinology, Department of medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan.
Jen-Chun WangDepartment of Emergency Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan.
Jaw-Wen ChenDivision of Cardiology, Department of Internal Medicine, Taipei Veterans General Hospital, Taipei, Taiwan.
Shing-Jong LinInstitute of Clinical Medicine, National Yang-Ming University, Taipei, Taiwan.
Tri-Service General Hospital · TWNational Yang Ming University Hospital · TWTaipei Veterans General Hospital · TWNational Defense Medical Center · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypoxia inducible factor-1α (HIF-1α) pathway is associated with many vascular diseases, including atherosclerosis, arterial aneurysms, pulmonary hypertension and chronic venous diseases. Significant HIF-1α expression could be found at the rupture edge at human abdominal aortic aneurysm (AAA) tissues. While our initial in vitro experiments had shown that deferoxamine (DFO) could attenuate angiotensin II (AngII) induced endothelial activations; we unexpectedly found that DFO augmented the severity of AngII-induced AAA, at least partly through increased accumulation of HIF-1α. The findings promoted us to test whether aneurysmal prone factors could up-regulate the expression of MMP-2 and MMP-9 through aberrantly increased HIF-1α and promote AAA development. AngII induced AAA in hyperlipidemic mice model was used. DFO, as a prolyl hydroxylase inhibitor, stabilized HIF-1α and augmented MMPs activities. Aneurysmal-prone factors induced HIF-1α can cause overexpression of MMP-2 and MMP-9 and promote aneurysmal progression. Pharmacological HIF-1α inhibitors, digoxin and 2-ME could ameliorate AngII induced AAA in vivo. HIF-1α is pivotal for the development of AAA. Our study provides a rationale for using HIF-1α inhibitors as an adjunctive medical therapy in addition to current cardiovascular risk-reducing regimens.

Indexed as

Down-RegulationGene Expression Regulation, EnzymologicAnimalsAortic Aneurysm, AbdominalCell LineDisease Models, AnimalHumansHypoxia-Inducible Factor 1, alpha SubunitMatrix Metalloproteinase 2Matrix Metalloproteinase 9MiceMice, KnockoutHif1a protein, mouseHypoxia-Inducible Factor 1, alpha SubunitMatrix Metalloproteinase 2Matrix Metalloproteinase 9Mmp2 protein, mouseMmp9 protein, mouse

Identifiers

PMID27363580
PMCPMC4929442
OpenAlexW2464748071

What OpenQuestion holds

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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.