Evidence map›Paper›PMID 17963039›Full record

ReviewNeurochemical research2008

11beta-HSD1, inflammation, metabolic disease and age-related cognitive (dys)function.

Karen E Chapman, Jonathan R Seckl

Abstract readReview
PubMed Publisher
In one paragraph

Review in Neurochemical research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

13 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Article
  3. Elevated hepatic 11β-hydroxysteroid dehydrogenase type 1 induces insulin resistance in uremia.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
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  6. Review
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  11. Glucocorticoid receptor haploinsufficiency causes hypertension and attenuates hypothalamic-pituitary-adrenal axis and blood pressure adaptions to high-fat diet.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2008
    Article
  12. Article
  13. 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

2 authors at 2 institutions in 1 country.

Karen E ChapmanEndocrinology Unit, Centre for Cardiovascular Sciences, Queen's Medical Research Institute, University of Edinburgh, 47 Little France Crescent, Edinburgh, EH16 4TJ, UK. Karen.Chapman@ed.ac.uk
Jonathan R Seckl
The Queen's Medical Research Institute · GBUniversity of Edinburgh · GB

Funding

British Heart FoundationMedical Research CouncilWellcome Trust
6 · The paper itself

Abstract

11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) is an intracellular amplifier of glucocorticoid action. By converting intrinsically inert glucocorticoids (cortisone, 11-dehydrocorticosterone) into their active forms (cortisol, corticosterone), 11beta-HSD1 increases glucocorticoid access to receptors. Glucocorticoid hormones modulate diverse physiological processes, linking circadian rhythms to food seeking, motivational and cognitive behaviours, as well as intermediary metabolism and immune responses. They are a key component of pathways that buffer the organism against stressful challenges. Here we review the part played in these processes by 11beta-HSD1, and discuss the promise of inhibitors of 11beta-HSD1 in alleviating disorders associated with cumulative stress.

Indexed as

11-beta-Hydroxysteroid Dehydrogenase Type 1AnimalsCognition DisordersGlucocorticoidsHumansInflammationMetabolic Diseases11-beta-Hydroxysteroid Dehydrogenase Type 1Glucocorticoids

Identifiers

PMID17963039
OpenAlexW2111182072

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.