Evidence map›Paper›PMID 32345536›Full record

ArticleRedox biology2020

Exacerbation of adverse cardiovascular effects of aircraft noise in an animal model of arterial hypertension.

Sebastian Steven, Katie Frenis, Sanela Kalinovic, Miroslava Kvandova, Matthias Oelze, Johanna Helmstädter, Omar Hahad, Konstantina Filippou, Kamil Kus, Chiara Trevisan and 9 more

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
11.1field-weighted citation impact, top 1% 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, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.

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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

19 authors at 7 institutions in 4 countries.

Sebastian StevenCenter for Cardiology, Cardiology I - Laboratory of Molecular Cardiology, University Medical Center of the Johannes Gutenberg-University, Mainz, Germany; Center for Thrombosis and Hemostasis, University Medical Center of the Johannes Gutenberg-University, Mainz, Germany.
Katie FrenisCenter for Cardiology, Cardiology I - Laboratory of Molecular Cardiology, University Medical Center of the Johannes Gutenberg-University, Mainz, Germany.
Sanela KalinovicCenter for Cardiology, Cardiology I - Laboratory of Molecular Cardiology, University Medical Center of the Johannes Gutenberg-University, Mainz, Germany.
Miroslava KvandovaCenter for Cardiology, Cardiology I - Laboratory of Molecular Cardiology, University Medical Center of the Johannes Gutenberg-University, Mainz, Germany.
Matthias OelzeCenter for Cardiology, Cardiology I - Laboratory of Molecular Cardiology, University Medical Center of the Johannes Gutenberg-University, Mainz, Germany.
Johanna HelmstädterCenter for Cardiology, Cardiology I - Laboratory of Molecular Cardiology, University Medical Center of the Johannes Gutenberg-University, Mainz, Germany.
Omar HahadCenter for Cardiology, Cardiology I - Laboratory of Molecular Cardiology, University Medical Center of the Johannes Gutenberg-University, Mainz, Germany; German Center for Cardiovascular Research (DZHK), Partner Site Rhine-Main, Mainz, Germany.
Konstantina FilippouCenter for Cardiology, Cardiology I - Laboratory of Molecular Cardiology, University Medical Center of the Johannes Gutenberg-University, Mainz, Germany.
Kamil KusJagiellonian Centre for Experimental Therapeutics (JCET), Jagiellonian University, Krakow, Poland.
Chiara TrevisanInstitute of Neuropathology, University Hospital, Zurich, Switzerland.
Klaus-Dieter SchlüterDepartment of Physiology, Justus-Liebig University Gießen, Germany.
Kerstin BoenglerDepartment of Physiology, Justus-Liebig University Gießen, Germany.
Stefan ChlopickiJagiellonian Centre for Experimental Therapeutics (JCET), Jagiellonian University, Krakow, Poland; Chair of Pharmacology, Jagiellonian University Medical College, Krakow, Poland.
Katrin FrauenknechtInstitute of Neuropathology, University Hospital, Zurich, Switzerland.
Rainer SchulzDepartment of Physiology, Justus-Liebig University Gießen, Germany.
Mette SorensenDanish Cancer Society, Copenhagen, Denmark; Department of Natural Science and Environment, Roskilde University, Roskilde, Denmark.
Andreas DaiberCenter for Cardiology, Cardiology I - Laboratory of Molecular Cardiology, University Medical Center of the Johannes Gutenberg-University, Mainz, Germany; German Center for Cardiovascular Research (DZHK), Partner Site Rhine-Main, Mainz, Germany. Electronic address: daiber@uni-mainz.de.
Swenja Kröller-SchönCenter for Cardiology, Cardiology I - Laboratory of Molecular Cardiology, University Medical Center of the Johannes Gutenberg-University, Mainz, Germany.
Thomas MünzelCenter for Cardiology, Cardiology I - Laboratory of Molecular Cardiology, University Medical Center of the Johannes Gutenberg-University, Mainz, Germany; German Center for Cardiovascular Research (DZHK), Partner Site Rhine-Main, Mainz, Germany. Electronic address: tmuenzel@uni-mainz.de.
Johannes Gutenberg University Mainz · DEJustus-Liebig-Universität Gießen · DEUniversity Medical Center of the Johannes Gutenberg University Mainz · DEGerman Centre for Cardiovascular Research · DEJagiellonian University · PLUniversity Hospital of Zurich · CHDanish Cancer Society · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Arterial hypertension is the most important risk factor for the development of cardiovascular disease. Recently, aircraft noise has been shown to be associated with elevated blood pressure, endothelial dysfunction, and oxidative stress. Here, we investigated the potential exacerbated cardiovascular effects of aircraft noise in combination with experimental arterial hypertension. C57BL/6J mice were infused with 0.5 mg/kg/d of angiotensin II for 7 days, exposed to aircraft noise for 7 days at a maximum sound pressure level of 85 dB(A) and a mean sound pressure level of 72 dB(A), or subjected to both stressors. Noise and angiotensin II increased blood pressure, endothelial dysfunction, oxidative stress and inflammation in aortic, cardiac and/or cerebral tissues in single exposure models. In mice subjected to both stressors, most of these risk factors showed potentiated adverse changes. We also found that mice exposed to both noise and ATII had increased phagocytic NADPH oxidase (NOX-2)-mediated superoxide formation, immune cell infiltration (monocytes, neutrophils and T cells) in the aortic wall, astrocyte activation in the brain, enhanced cytokine signaling, and subsequent vascular and cerebral oxidative stress. Exaggerated renal stress response was also observed. In summary, our results show an enhanced adverse cardiovascular effect between environmental noise exposure and arterial hypertension, which is mainly triggered by vascular inflammation and oxidative stress. Mechanistically, noise potentiates neuroinflammation and cerebral oxidative stress, which may be a potential link between both risk factors. The results indicate that a combination of classical (arterial hypertension) and novel (noise exposure) risk factors may be deleterious for cardiovascular health.

Indexed as

Endothelium, VascularHypertensionAircraftAnimalsBlood PressureMiceMice, Inbred C57BLOxidative StressArterial hypertensionEndothelial functionEnvironmental noise exposureInflammationVascular oxidative stress

Identifiers

PMID32345536
PMCPMC7327989
OpenAlexW3017190878

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.