Evidence map›Paper›PMID 34439486›Full record

ArticleAntioxidants (Basel, Switzerland)2021

Angiotensin II Induces Oxidative Stress and Endothelial Dysfunction in Mouse Ophthalmic Arteries via Involvement of AT1 Receptors and NOX2.

Michael Birk, Ewa Baum, Jenia Kouchek Zadeh, Caroline Manicam, Norbert Pfeiffer, Andreas Patzak, Johanna Helmstädter, Sebastian Steven, Marin Kuntic, Andreas Daiber and 1 more

Abstract read
In one paragraph

Article in Antioxidants (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
–field-weighted citation impact
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

25 citing papers in PubMed.

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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

11 authors.

Michael BirkDepartment of Ophthalmology, University Medical Center, Johannes Gutenberg University Mainz, Langenbeckstrasse 1, 55131 Mainz, Germany.
Ewa BaumDepartment of Ophthalmology, University Medical Center, Johannes Gutenberg University Mainz, Langenbeckstrasse 1, 55131 Mainz, Germany.
Jenia Kouchek ZadehDepartment of Ophthalmology, University Medical Center, Johannes Gutenberg University Mainz, Langenbeckstrasse 1, 55131 Mainz, Germany.
Caroline ManicamDepartment of Ophthalmology, University Medical Center, Johannes Gutenberg University Mainz, Langenbeckstrasse 1, 55131 Mainz, Germany.ORCID 0000-0001-5891-1155
Norbert PfeifferDepartment of Ophthalmology, University Medical Center, Johannes Gutenberg University Mainz, Langenbeckstrasse 1, 55131 Mainz, Germany.
Andreas PatzakInstitute of Vegetative Physiology, Charité-Universitätsmedizin Berlin, Charitéplatz 1, 10117 Berlin, Germany.ORCID 0000-0002-1088-6875
Johanna HelmstädterDepartment of Cardiology, Cardiology I-Laboratory of Molecular Cardiology, University Medical Center, Johannes Gutenberg University, Building 605, Langenbeckstr. 1, 55131 Mainz, Germany.
Sebastian StevenDepartment of Cardiology, Cardiology I-Laboratory of Molecular Cardiology, University Medical Center, Johannes Gutenberg University, Building 605, Langenbeckstr. 1, 55131 Mainz, Germany.ORCID 0000-0002-5332-9294
Marin KunticDepartment of Cardiology, Cardiology I-Laboratory of Molecular Cardiology, University Medical Center, Johannes Gutenberg University, Building 605, Langenbeckstr. 1, 55131 Mainz, Germany.
Andreas DaiberDepartment of Cardiology, Cardiology I-Laboratory of Molecular Cardiology, University Medical Center, Johannes Gutenberg University, Building 605, Langenbeckstr. 1, 55131 Mainz, Germany.ORCID 0000-0002-2769-0094
Adrian GerickeDepartment of Ophthalmology, University Medical Center, Johannes Gutenberg University Mainz, Langenbeckstrasse 1, 55131 Mainz, Germany.ORCID 0000-0002-3506-8465

Funding

Deutsche Forschungsgemeinschaft STE2528/2-1
6 · The paper itself

Abstract

Angiotensin II (Ang II) has been implicated in the pathophysiology of various age-dependent ocular diseases. The purpose of this study was to test the hypothesis that Ang II induces endothelial dysfunction in mouse ophthalmic arteries and to identify the underlying mechanisms. Ophthalmic arteries were exposed to Ang II in vivo and in vitro to determine vascular function by video microscopy. Moreover, the formation of reactive oxygen species (ROS) was quantified and the expression of prooxidant redox genes and proteins was determined. The endothelium-dependent artery responses were blunted after both in vivo and in vitro exposure to Ang II. The Ang II type 1 receptor (AT1R) blocker, candesartan, and the ROS scavenger, Tiron, prevented Ang II-induced endothelial dysfunction. ROS levels and NOX2 expression were increased following Ang II incubation. Remarkably, Ang II failed to induce endothelial dysfunction in ophthalmic arteries from NOX2-deficient mice. Following Ang II incubation, endothelium-dependent vasodilation was mainly mediated by cytochrome P450 oxygenase (CYP450) metabolites, while the contribution of nitric oxide synthase (NOS) and 12/15-lipoxygenase (12/15-LOX) pathways became negligible. These findings provide evidence that Ang II induces endothelial dysfunction in mouse ophthalmic arteries via AT1R activation and NOX2-dependent ROS formation. From a clinical point of view, the blockade of AT1R signaling and/or NOX2 may be helpful to retain or restore endothelial function in ocular blood vessels in certain ocular diseases.

Indexed as

angiotensin IIendothelial dysfunctionophthalmic arteryoxidative stress

Identifiers

PMID34439486
PMCPMC8389243

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.