Evidence map›Paper›PMID 23899562›Full record

ReviewPhysiological reviews2013

11β-hydroxysteroid dehydrogenases: intracellular gate-keepers of tissue glucocorticoid action.

Karen Chapman, Megan Holmes, Jonathan Seckl

Open access · greenAbstract readReview
In one paragraph

Review in Physiological reviews, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 402 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
402citing papers in PubMed, 2 pooled it
33.9field-weighted citation impact, top 1% 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

402 citing papers in PubMed, 2 syntheses or guidelines pooled it, 850 citations in OpenAlex.

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  17. Glucocorticoid trajectories in preterm infants-born too soon, wired differently.The Journal of clinical endocrinology and metabolism · 2026
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342 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

3 authors at 2 institutions in 1 country.

Karen ChapmanEndocrinology Unit, Centre for Cardiovascular Science, The Queen’s Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom.
Megan Holmes
Jonathan Seckl
University of Edinburgh · GBThe Queen's Medical Research Institute · GB

Funding

British Heart FoundationMedical Research Council G0800235Medical Research Council MR/K026992/1Wellcome Trust
6 · The paper itself

Abstract

Glucocorticoid action on target tissues is determined by the density of "nuclear" receptors and intracellular metabolism by the two isozymes of 11β-hydroxysteroid dehydrogenase (11β-HSD) which catalyze interconversion of active cortisol and corticosterone with inert cortisone and 11-dehydrocorticosterone. 11β-HSD type 1, a predominant reductase in most intact cells, catalyzes the regeneration of active glucocorticoids, thus amplifying cellular action. 11β-HSD1 is widely expressed in liver, adipose tissue, muscle, pancreatic islets, adult brain, inflammatory cells, and gonads. 11β-HSD1 is selectively elevated in adipose tissue in obesity where it contributes to metabolic complications. Similarly, 11β-HSD1 is elevated in the ageing brain where it exacerbates glucocorticoid-associated cognitive decline. Deficiency or selective inhibition of 11β-HSD1 improves multiple metabolic syndrome parameters in rodent models and human clinical trials and similarly improves cognitive function with ageing. The efficacy of inhibitors in human therapy remains unclear. 11β-HSD2 is a high-affinity dehydrogenase that inactivates glucocorticoids. In the distal nephron, 11β-HSD2 ensures that only aldosterone is an agonist at mineralocorticoid receptors (MR). 11β-HSD2 inhibition or genetic deficiency causes apparent mineralocorticoid excess and hypertension due to inappropriate glucocorticoid activation of renal MR. The placenta and fetus also highly express 11β-HSD2 which, by inactivating glucocorticoids, prevents premature maturation of fetal tissues and consequent developmental "programming." The role of 11β-HSD2 as a marker of programming is being explored. The 11β-HSDs thus illuminate the emerging biology of intracrine control, afford important insights into human pathogenesis, and offer new tissue-restricted therapeutic avenues.

Indexed as

11-beta-Hydroxysteroid DehydrogenasesAnimalsGene Expression Regulation, EnzymologicGlucocorticoidsHumansReceptors, GlucocorticoidReceptors, MineralocorticoidTissue Distribution11-beta-Hydroxysteroid DehydrogenasesGlucocorticoidsReceptors, GlucocorticoidReceptors, Mineralocorticoid

Identifiers

PMID23899562
PMCPMC3962546
OpenAlexW2152760742

What OpenQuestion holds

Textmetadata
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.