Evidence map›Paper›PMID 32463582›Full record

ArticleAging cell2020

Altered glucocorticoid metabolism represents a feature of macroph-aging.

Jenny Vanessa Valbuena Perez, Rebecca Linnenberger, Anna Dembek, Stefano Bruscoli, Carlo Riccardi, Marcel H Schulz, Markus R Meyer, Alexandra K Kiemer, Jessica Hoppstädter

Open access · goldAbstract read
In one paragraph

Article in Aging cell, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 2 pooled it
2.6field-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

24 citing papers in PubMed, 2 syntheses or guidelines pooled it, 39 citations in OpenAlex.

  1. Infertility and cortisol: a systematic review.Frontiers in endocrinology · 2023
    Pooled it
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  10. Pharmacology of Aging:Aging biology · 2024
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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

9 authors at 3 institutions in 2 countries.

Jenny Vanessa Valbuena PerezPharmaceutical Biology, Department of Pharmacy, Saarland University, Saarbrücken, Germany.
Rebecca LinnenbergerPharmaceutical Biology, Department of Pharmacy, Saarland University, Saarbrücken, Germany.
Anna DembekPharmaceutical Biology, Department of Pharmacy, Saarland University, Saarbrücken, Germany.
Stefano BruscoliPharmacology, Department of Medicine, Perugia University, Perugia, Italy.
Carlo RiccardiPharmacology, Department of Medicine, Perugia University, Perugia, Italy.
Marcel H SchulzInstitute for Cardiovascular Regeneration, Goethe University, Frankfurt am Main, Germany.
Markus R MeyerDepartment of Experimental and Clinical Toxicology, Institute of Experimental and Clinical Pharmacology and Toxicology, Center for Molecular Signaling (PZMS), Saarland University, Homburg, Germany.
Alexandra K KiemerPharmaceutical Biology, Department of Pharmacy, Saarland University, Saarbrücken, Germany.ORCID 0000-0002-7224-9900
Jessica HoppstädterPharmaceutical Biology, Department of Pharmacy, Saarland University, Saarbrücken, Germany.ORCID 0000-0001-8758-1554
Saarland University · DEUniversity of Perugia · ITGoethe University Frankfurt · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The aging process is characterized by a chronic, low-grade inflammatory state, termed "inflammaging." It has been suggested that macrophage activation plays a key role in the induction and maintenance of this state. In the present study, we aimed to elucidate the mechanisms responsible for aging-associated changes in the myeloid compartment of mice. The aging phenotype, characterized by elevated cytokine production, was associated with a dysfunction of the hypothalamic-pituitary-adrenal (HPA) axis and diminished serum corticosteroid levels. In particular, the concentration of corticosterone, the major active glucocorticoid in rodents, was decreased. This could be explained by an impaired expression and activity of 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1), an enzyme that determines the extent of cellular glucocorticoid responses by reducing the corticosteroids cortisone/11-dehydrocorticosterone to their active forms cortisol/corticosterone, in aged macrophages and peripheral leukocytes. These changes were accompanied by a downregulation of the glucocorticoid receptor target gene glucocorticoid-induced leucine zipper (GILZ) in vitro and in vivo. Since GILZ plays a central role in macrophage activation, we hypothesized that the loss of GILZ contributed to the process of macroph-aging. The phenotype of macrophages from aged mice was indeed mimicked in young GILZ knockout mice. In summary, the current study provides insight into the role of glucocorticoid metabolism and GILZ regulation during aging.

Indexed as

Age FactorsAnimalsCytokinesDisease Models, AnimalGlucocorticoidsInflammationMacrophage ActivationMacrophages, PeritonealMiceMice, Inbred C57BLMice, KnockoutReactive Oxygen SpeciesCytokinesGlucocorticoidsReactive Oxygen Speciescellular immunologycytokinesinflammationmononuclear cellmouse modelsreactive oxygen speciessteroid control of agingTSC22D3

Identifiers

PMID32463582
PMCPMC7294787
OpenAlexW3030846944

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.