Evidence map›Paper›PMID 31795255›Full record

ReviewInternational journal of molecular sciences2019

Role of the Aryl Hydrocarbon Receptor in Environmentally Induced Skin Aging and Skin Carcinogenesis.

Christian Vogeley, Charlotte Esser, Thomas Tüting, Jean Krutmann, Thomas Haarmann-Stemmann

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
9.3field-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

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 83 citations in OpenAlex.

  1. Pooled it
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  7. Harnessing Quinone Derivatives fromACS pharmacology & translational science · 2025
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  20. Photoaging: UV radiation-induced inflammation and immunosuppression accelerate the aging process in the skin.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022
    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

5 authors at 2 institutions in 1 country.

Christian VogeleyIUF-Leibniz-Research Institute for Environmental Medicine, 40225 Düsseldorf, Germany.
Charlotte EsserIUF-Leibniz-Research Institute for Environmental Medicine, 40225 Düsseldorf, Germany.
Thomas TütingLaboratory of Experimental Dermatology, Department of Dermatology, Otto-von-Guericke University, 39120 Magdeburg, Germany.
Jean KrutmannIUF-Leibniz-Research Institute for Environmental Medicine, 40225 Düsseldorf, Germany.
Thomas Haarmann-StemmannIUF-Leibniz-Research Institute for Environmental Medicine, 40225 Düsseldorf, Germany.
Leibniz Institute of Environmental Medicine · DEOtto-von-Guericke University Magdeburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The skin is constantly exposed to a variety of environmental threats, including solar electromagnetic radiation, microbes, airborne particulate matter, and chemicals. Acute exposure to these environmental factors results in the activation of different signaling pathways that orchestrate adaptive stress responses to maintain cell and tissue homeostasis. Chronic exposure of skin to these factors, however, may lead to the accumulation of damaged macromolecules and loss of cell and tissue integrity, which, over time, may facilitate aging processes and the development of aging-related malignancies. One transcription factor that is expressed in all cutaneous cells and activated by various environmental stressors, including dioxins, polycyclic aromatic hydrocarbons, and ultraviolet radiation, is the aryl hydrocarbon receptor (AHR). By regulating keratinocyte proliferation and differentiation, epidermal barrier function, melanogenesis, and immunity, a certain degree of AHR activity is critical to maintain skin integrity and to adapt to acute stress situations. In contrast, a chronic activation of cutaneous AHR signaling critically contributes to premature aging and the development of neoplasms by affecting metabolism, extracellular matrix remodeling, inflammation, pigmentation, DNA repair, and apoptosis. This article provides an overview of the detrimental effects associated with sustained AHR activity in chronically stressed skin and pinpoints AHR as a promising target for chemoprevention.

Indexed as

Environmental ExposureSkin AgingAnimalsExtracellular MatrixHumansReceptors, Aryl HydrocarbonSkin NeoplasmsReceptors, Aryl HydrocarbonDNA damageextracellular matrixextrinsic skin agingmelanomaparticulate matterpigmentationpolycyclic aromatic hydrocarbonssquamous cell carcinomaUV radiation

Identifiers

PMID31795255
PMCPMC6928879
OpenAlexW2989793350

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.