Evidence map›Paper›PMID 25804222›Full record

ReviewThe Journal of steroid biochemistry and molecular biology2015

Glucocorticoid signaling in the heart: A cardiomyocyte perspective.

Robert H Oakley, John A Cidlowski

Open access · greenAbstract readReview
In one paragraph

Review in The Journal of steroid biochemistry and molecular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed
6.9field-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

76 citing papers in PubMed, 116 citations in OpenAlex.

  1. Acute cardiovascular manifestations of hypocortisolism.World journal of emergency medicine · 2026
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  11. Influence of stressful life events and personality traits on PLN cardiomyopathy severity: an exploratory study.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2023
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  17. A rare homozygous variant ofFrontiers in endocrinology · 2023
    Article
  18. Review
  19. Article
  20. Article

16 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Robert H OakleyLaboratory of Signal Transduction, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, 111 TW Alexander Drive, P.O. Box 12233, MD F3-07, Research Triangle Park, North Carolina 27709, USA. Electronic address: oakleyr2@niehs.nih.gov.
John A CidlowskiLaboratory of Signal Transduction, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, 111 TW Alexander Drive, P.O. Box 12233, MD F3-07, Research Triangle Park, North Carolina 27709, USA. Electronic address: cidlows1@niehs.nih.gov.
National Institutes of Health · US

Funding

Glucocorticoid Hormone ActionZIAES090057 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI CIDLOWSKI, JOHN A. · 2009 to 2025
$44.9M
Intramural NIH HHS Z99 ES999999
6 · The paper itself

Abstract

Heart failure is one of the leading causes of death in the Western world. Glucocorticoids are primary stress hormones that regulate a vast array of biological processes, and synthetic derivatives of these steroids have been mainstays in the clinic for the last half century. Abnormal levels of glucocorticoids are known to negatively impact the cardiovascular system; however, surprisingly little is known about the direct role of glucocorticoid signaling in the heart. The actions of glucocorticoids are mediated classically by the glucocorticoid receptor (GR). In certain cells, such as cardiomyocytes, glucocorticoid occupancy and activation of the mineralocorticoid receptor (MR) may also contribute to the observed response. Recently, there has been a surge of reports investigating the in vivo function of glucocorticoid signaling in the heart using transgenic mice that specifically target GR or MR in cardiomyocytes. Results from these studies suggest that GR signaling in cardiomyocytes is critical for the normal development and function of the heart. In contrast, MR signaling in cardiomyocytes participates in the development and progression of cardiac disease. In the following review, we discuss these genetic mouse models and the new insights they are providing into the direct role cardiomyocyte glucocorticoid signaling plays in heart physiology and pathophysiology. This article is part of a Special Issue entitled 'Steroid Perspectives'.

Indexed as

Signal TransductionAnimalsGlucocorticoidsHeartHeart DiseasesHumansMiceMice, TransgenicMyocardiumMyocytes, CardiacReceptors, GlucocorticoidReceptors, MineralocorticoidGlucocorticoidsReceptors, GlucocorticoidReceptors, MineralocorticoidCardiomyocytesGlucocorticoid receptorGlucocorticoidsMineralocorticoid receptorTransgenic mice

Identifiers

PMID25804222
PMCPMC4568128
OpenAlexW2085727131

What OpenQuestion holds

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LicenceTDM
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.