Evidence map›Paper›PMID 27626316›Full record

ArticleOncotarget2016

Heme oxygenase-1 deficiency exacerbates angiotensin II-induced aortic aneurysm in mice.

Yen-Chun Ho, Meng-Ling Wu, Pei-Yu Gung, Chung-Huang Chen, Cheng-Chin Kuo, Shaw-Fang Yet

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

30 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
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  4. Dihydromyricetin mitigates abdominal aortic aneurysmActa pharmaceutica Sinica. B · 2025
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  11. Review
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  14. Review
  15. The Modulation of Nrf-2/HO-1 Signaling Axis byPlants (Basel, Switzerland) · 2021
    Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review
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 2 institutions in 1 country.

Yen-Chun HoInstitute of Cellular and System Medicine, National Health Research Institutes, Zhunan, Taiwan.
Meng-Ling WuInstitute of Cellular and System Medicine, National Health Research Institutes, Zhunan, Taiwan.
Pei-Yu GungInstitute of Cellular and System Medicine, National Health Research Institutes, Zhunan, Taiwan.
Chung-Huang ChenInstitute of Cellular and System Medicine, National Health Research Institutes, Zhunan, Taiwan.
Cheng-Chin KuoInstitute of Cellular and System Medicine, National Health Research Institutes, Zhunan, Taiwan.
Shaw-Fang YetInstitute of Cellular and System Medicine, National Health Research Institutes, Zhunan, Taiwan.
National Health Research Institutes · TWNational Defense Medical Center · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Abdominal aortic aneurysm (AAA) is a chronic but often fatal disease in elderly population. Heme oxygenase-1 (HO-1) is a stress response protein with antioxidative and anti-inflammatory properties. HO-1 has been shown to protect against atherogenesis and arterial intimal thickening. Emerging evidences suggest that AAA and arterial occlusive disease have distinct pathogenic mechanisms. Thus, in this study we investigated the role of HO-1 in angiotensin II-induced AAA formation in HO-1+/+apoE-/- and HO-1-/-apoE-/- mice. We found that complete loss of HO-1 increased AAA incidence and rupture rate, and drastically increased aneurysmal area and severity, accompanied with severe elastin degradation and medial degeneration. Interestingly, we often observed not only AAA but also thoracic aortic aneurysm in HO-1-/-apoE-/- mice. Furthermore, reactive oxygen species levels, vascular smooth muscle cell (VSMC) loss, macrophage infiltration, matrix metalloproteinase (MMP) activity were markedly enhanced in the aneurysmal aortic wall in HO-1-/-apoE-/- mice. In addition, HO-1-/-apoE-/- VSMCs were more susceptible to oxidant-induced cell death and macrophages from HO-1-/-apoE-/- mice had aggravated responses to angiotensin II with substantial increases in inflammatory cytokine productions and MMP9 activity. Taken together, our results demonstrate the essential roles of HO-1 in suppressing the pathogenesis of AAA. Targeting HO-1 might be a promising therapeutic strategy for AAA.

Indexed as

Anemia, HemolyticAngiotensin IIAnimalsAorta, AbdominalAortic Aneurysm, AbdominalCytokinesGrowth DisordersHeme Oxygenase-1Iron Metabolism DisordersMaleMatrix Metalloproteinase 9Mice, Inbred C57BLMice, KnockoutReactive Oxygen SpeciesAngiotensin IICytokinesHeme Oxygenase-1Matrix Metalloproteinase 9Reactive Oxygen Speciesabdominalaortic aneurysmheme oxygenase-1inflammationoxidative stressPathology Section

Identifiers

PMID27626316
PMCPMC5356517
OpenAlexW2516931782

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.