Evidence map›Paper›PMID 19239478›Full record

ReviewBritish journal of pharmacology2009

Therapeutic manipulation of glucocorticoid metabolism in cardiovascular disease.

Patrick W F Hadoke, Javaid Iqbal, Brian R Walker

Open access · bronzeAbstract readReview
In one paragraph

Review in British journal of pharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

48 citing papers in PubMed, 98 citations in OpenAlex.

  1. Trial
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  10. Cortisol and cardiometabolic disease: a target for advancing health equity.Trends in endocrinology and metabolism: TEM · 2022
    Review
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  19. Definitions and pathophysiology of vasoplegic shock.Critical care (London, England) · 2018
    Review
  20. Article
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.

Patrick W F HadokeCentre for Cardiovascular Sciences, University of Edinburgh, The Queen's Medical Research Institute, Edinburgh, UK. phadoke@staffmail.ed.ac.uk
Javaid Iqbal
Brian R Walker
The Queen's Medical Research Institute · GBUniversity of Edinburgh · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The therapeutic potential for manipulation of glucocorticoid metabolism in cardiovascular disease was revolutionized by the recognition that access of glucocorticoids to their receptors is regulated in a tissue-specific manner by the isozymes of 11beta-hydroxysteroid dehydrogenase. Selective inhibitors of 11beta-hydroxysteroid dehydrogenase type 1 have been shown recently to ameliorate cardiovascular risk factors and inhibit the development of atherosclerosis. This article addresses the possibility that inhibition of 11beta-hydroxsteroid dehydrogenase type 1 activity in cells of the cardiovascular system contributes to this beneficial action. The link between glucocorticoids and cardiovascular disease is complex as glucocorticoid excess is linked with increased cardiovascular events but glucocorticoid administration can reduce atherogenesis and restenosis in animal models. There is considerable evidence that glucocorticoids can interact directly with cells of the cardiovascular system to alter their function and structure and the inflammatory response to injury. These actions may be regulated by glucocorticoid and/or mineralocorticoid receptors but are also dependent on the 11beta-hydroxysteroid dehydrogenases which may be expressed in cardiac, vascular (endothelial, smooth muscle) and inflammatory (macrophages, neutrophils) cells. The activity of 11beta-hydroxysteroid dehydrogenases in these cells is dependent upon differentiation state, the action of pro-inflammaotory cytokines and the influence of endogenous inhibitors (oxysterols, bile acids). Further investigations are required to clarify the link between glucocorticoid excess and cardiovascular events and to determine the mechanism through which glucocorticoid treatment inhibits atherosclerosis/restenosis. This will provide greater insights into the potential benefit of selective 11beta-hydroxysteroid dehydrogenase inhibitors in treatment of cardiovascular disease.

Indexed as

11-beta-Hydroxysteroid DehydrogenasesAnimalsAtherosclerosisBlood VesselsCardiovascular DiseasesGlucocorticoidsHumansMuscle, Smooth, VascularMyocardiumOrgan SpecificityReceptors, GlucocorticoidReceptors, MineralocorticoidTunica Intima11-beta-Hydroxysteroid DehydrogenasesGlucocorticoidsReceptors, GlucocorticoidReceptors, Mineralocorticoid

Identifiers

PMID19239478
PMCPMC2697748
OpenAlexW1550426019

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.