Evidence map›Paper›PMID 40346507›Full record

ArticleBMC genomics2025

A cross-tissue transcriptomic approach decodes glucocorticoid receptor-dependent links to human metabolic phenotypes.

Marcin Piechota, Mateusz Zieba, Małgorzata Borczyk, Slawomir Golda, Jacek Hajto, Urszula Skupio, Michal Slezak, Jan Rodriguez Parkitna, Michal Korostynski

Abstract read
In one paragraph

Article in BMC genomics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Review
  2. Review
  3. 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

9 authors.

Marcin PiechotaLaboratory of Pharmacogenomics, Maj Institute of Pharmacology, Polish Academy of Sciences, Krakow, 31-343, Poland.
Mateusz ZiebaLaboratory of Pharmacogenomics, Maj Institute of Pharmacology, Polish Academy of Sciences, Krakow, 31-343, Poland.
Małgorzata BorczykLaboratory of Pharmacogenomics, Maj Institute of Pharmacology, Polish Academy of Sciences, Krakow, 31-343, Poland.
Slawomir GoldaDepartment of Molecular Neuropharmacology, Maj Institute of Pharmacology, Polish Academy of Sciences, Krakow, 31-343, Poland.
Jacek HajtoLaboratory of Pharmacogenomics, Maj Institute of Pharmacology, Polish Academy of Sciences, Krakow, 31-343, Poland.
Urszula SkupioDepartment of Molecular Neuropharmacology, Maj Institute of Pharmacology, Polish Academy of Sciences, Krakow, 31-343, Poland.
Michal SlezakLukasiewicz Research Network - PORT Polish Center for Technology Development, Wroclaw, 54-066, Poland.
Jan Rodriguez ParkitnaDepartment of Molecular Neuropharmacology, Maj Institute of Pharmacology, Polish Academy of Sciences, Krakow, 31-343, Poland.
Michal KorostynskiLaboratory of Pharmacogenomics, Maj Institute of Pharmacology, Polish Academy of Sciences, Krakow, 31-343, Poland. michkor@if-pan.krakow.pl.ORCID http://orcid.org/0000-0002-4273-7401

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glucocorticoids, acting through the glucocorticoid receptor (GR), control metabolism, maintain homeostasis, and enable adaptive responses to environmental challenges. Their function has been comprehensively studied, leading to identification of numerous tissue-specific GR-dependent mechanisms. Abundant evidence shows that GR-triggered responses differ across tissues, however, the extent of this specificity was not comprehensively explored. It is also unknown how particular GR-induced molecular patterns are translated into profile of higher-level human traits. Here, we examine cross-tissue effects of GR activation on gene expression. We assessed changes induced by stimulation with GR agonist, dexamethasone in nine tissues (adrenal cortex, perigonadal adipose tissue, hypothalamus, liver, kidney, anterior thigh muscle, pituitary gland, spleen, and lungs) in adult male C57BL/6 mice, using whole-genome microarrays. Dexamethasone induced balanced transcriptional responses across all examined tissues with 585 identified dexamethasone-regulated transcripts, including 446 with significant treatment-tissue interaction effects. Clustering analysis revealed sixteen GR-dependent patterns, including those universal across tissues and tissue-specific. We leveraged existing gene annotations and created new annotation sets based on chromatin immunoprecipitation sequencing, recent large-scale genome-wide association studies, and human transcriptome collections. As expected, GR-dependent transcripts were associated with essential metabolic processes (glycolysis/gluconeogenesis, lipid-metabolism) and inflammation-related pathways. Beyond these, we found novel links between regulated gene patterns and human phenotypic traits, like reticulocyte count or blood triglyceride levels. Overall effects of GR stimulation are well coordinated and closely linked to biological roles of tissues and organs. Our findings provide novel insights into complex systemic and tissue-specific actions of glucocorticoids and their potential impacts on human physiology and pathology.

Indexed as

Gene Expression ProfilingReceptors, GlucocorticoidTranscriptomeAnimalsDexamethasoneGlucocorticoidsHumansMaleMiceMice, Inbred C57BLOrgan SpecificityPhenotypeDexamethasoneGlucocorticoidsReceptors, GlucocorticoidDexamethasoneGlucocorticoid receptorMetabolic traitsTissue-specific transcriptionTranscriptional regulation

Identifiers

PMID40346507
PMCPMC12063231

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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.