Evidence map›Paper›PMID 26790370›Full record

ArticleScientific reports2016

The aryl hydrocarbon receptor promotes aging phenotypes across species.

Anna Eckers, Sascha Jakob, Christian Heiss, Thomas Haarmann-Stemmann, Christine Goy, Vanessa Brinkmann, Miriam M Cortese-Krott, Roberto Sansone, Charlotte Esser, Niloofar Ale-Agha and 3 more

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 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

53 citing papers in PubMed, 89 citations in OpenAlex.

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  19. The Aryl Hydrocarbon Receptor, Epigenetics and the Aging Process.The journal of nutrition, health & aging · 2023
    Article
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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

13 authors at 2 institutions in 1 country.

Anna EckersIUF-Leibniz Research Institute for Environmental Medicine, 40225 Duesseldorf, Germany.
Sascha JakobIUF-Leibniz Research Institute for Environmental Medicine, 40225 Duesseldorf, Germany.
Christian HeissDivision of Cardiology, Pulmonary Diseases, Vascular Medicine, Medical Faculty, University Duesseldorf, 40225 Duesseldorf, Germany.
Thomas Haarmann-StemmannIUF-Leibniz Research Institute for Environmental Medicine, 40225 Duesseldorf, Germany.
Christine GoyIUF-Leibniz Research Institute for Environmental Medicine, 40225 Duesseldorf, Germany.
Vanessa BrinkmannIUF-Leibniz Research Institute for Environmental Medicine, 40225 Duesseldorf, Germany.
Miriam M Cortese-KrottDivision of Cardiology, Pulmonary Diseases, Vascular Medicine, Medical Faculty, University Duesseldorf, 40225 Duesseldorf, Germany.
Roberto SansoneDivision of Cardiology, Pulmonary Diseases, Vascular Medicine, Medical Faculty, University Duesseldorf, 40225 Duesseldorf, Germany.
Charlotte EsserIUF-Leibniz Research Institute for Environmental Medicine, 40225 Duesseldorf, Germany.
Niloofar Ale-AghaIUF-Leibniz Research Institute for Environmental Medicine, 40225 Duesseldorf, Germany.
Joachim AltschmiedIUF-Leibniz Research Institute for Environmental Medicine, 40225 Duesseldorf, Germany.
Natascia VenturaCentral Institute of Clinical Chemistry and Laboratory Medicine, Medical Faculty, University of Duesseldorf, 40225 Duesseldorf, Germany.
Judith HaendelerCentral Institute of Clinical Chemistry and Laboratory Medicine, Medical Faculty, University of Duesseldorf, 40225 Duesseldorf, Germany.
Leibniz Institute of Environmental Medicine · DEHeinrich Heine University Düsseldorf · DE

Funding

Enhancing and expanding the CGC Strain CollectionP40OD010440 · OD · UNIVERSITY OF MINNESOTA · PI Aric L Daul, Ann E. Rougvie · 2012 to 2026
$7.5M
NIH HHS P40 OD010440
6 · The paper itself

Abstract

The ubiquitously expressed aryl hydrocarbon receptor (AhR) induces drug metabolizing enzymes as well as regulators of cell growth, differentiation and apoptosis. Certain AhR ligands promote atherosclerosis, an age-associated vascular disease. Therefore, we investigated the role of AhR in vascular functionality and aging. We report a lower pulse wave velocity in young and old AhR-deficient mice, indicative of enhanced vessel elasticity. Moreover, endothelial nitric oxide synthase (eNOS) showed increased activity in the aortas of these animals, which was reflected in increased NO production. Ex vivo, AhR activation reduced the migratory capacity of primary human endothelial cells. AhR overexpression as well as treatment with a receptor ligand, impaired eNOS activation and reduced S-NO content. All three are signs of endothelial dysfunction. Furthermore, AhR expression in blood cells of healthy human volunteers positively correlated with vessel stiffness. In the aging model Caenorhabditis elegans, AhR-deficiency resulted in increased mean life span, motility, pharynx pumping and heat shock resistance, suggesting healthier aging. Thus, AhR seems to have a negative impact on vascular and organismal aging. Finally, our data from human subjects suggest that AhR expression levels could serve as an additional, new predictor of vessel aging.

Indexed as

PhenotypeAdultAgedAge FactorsAgingAnimalsApoptosisCaenorhabditis elegansCell LineCell MovementCell ProliferationEndothelial CellsGene ExpressionHumansLongevityMiceNitric OxideNitric Oxide Synthase Type IIIReceptors, Aryl Hydrocarbon

Identifiers

PMID26790370
PMCPMC4726214
OpenAlexW2259018153

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.