Evidence map›Paper›PMID 17965745›Full record

ReviewBritish journal of pharmacology2008

The endothelin system as a therapeutic target in cardiovascular disease: great expectations or bleak house?

N S Kirkby, P W F Hadoke, A J Bagnall, D J Webb

Open access · bronzeAbstract readReview
In one paragraph

Review in British journal of pharmacology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
11.1field-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

62 citing papers in PubMed, 176 citations in OpenAlex.

  1. Inflammatory Biomarkers Predict Domain-Specific Cognitive Decline in Older Adults.The journals of gerontology. Series A, Biological sciences and medical sciences · 2017
    Trial
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  7. Endothelial cell dysfunction in cardiac disease: driver or consequence?Frontiers in cell and developmental biology · 2023
    Review
  8. A bioassay system of autologous human endothelial, smooth muscle cells, and leukocytes for use in drug discovery, phenotyping, and tissue engineering.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    Article
  9. G protein-coupled receptor 37L1 regulates renal sodium transport and blood pressure.American journal of physiology. Renal physiology · 2019
    Article
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  12. Article
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2 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

4 authors at 2 institutions in 1 country.

N S KirkbyCentre for Cardiovascular Science, The Queen's Medical Research Institute, University of Edinburgh, Edinburgh, Scotland, UK.
P W F Hadoke
A J Bagnall
D J Webb
The Queen's Medical Research Institute · GBUniversity of Edinburgh · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

There is considerable evidence that the potent vasoconstrictor endothelin-1 (ET-1) contributes to the pathogenesis of a variety of cardiovascular diseases. As such, pharmacological manipulation of the ET system might represent a promising therapeutic goal. Many clinical trials have assessed the potential of ET receptor antagonists in cardiovascular disease, the most positive of which have resulted in the licensing of the mixed ET receptor antagonist bosentan, and the selective ET(A) receptor antagonists, sitaxsentan and ambrisentan, for the treatment of pulmonary arterial hypertension (PAH). In contrast, despite encouraging data from in vitro and animal studies, outcomes in human heart failure have been disappointing, perhaps illustrating the risk of extrapolating preclinical work to man. Many further potential applications of these compounds, including resistant hypertension, chronic kidney disease, connective tissue disease and sub-arachnoid haemorrhage are currently being investigated in the clinic. Furthermore, experience from previous studies should enable improved trial design and scope remains for development of improved compounds and alternative therapeutic strategies. Although ET-converting enzyme inhibitors may represent one such alternative, there have been relatively few suitable compounds developed, and consequently, clinical experience with these agents remains extremely limited. Recent advances, together with an increased understanding of the biology of the ET system provided by improved experimental tools (including cell-specific transgenic deletion of ET receptors), should allow further targeting of clinical trials to diseases in which ET is involved and allow the therapeutic potential for targeting the ET system in cardiovascular disease to be fully realized.

Indexed as

Drug Delivery SystemsEndothelin Receptor AntagonistsAnimalsAspartic Acid EndopeptidasesCardiovascular DiseasesControlled Clinical Trials as TopicEndothelin-1Endothelin-Converting EnzymesEnzyme InhibitorsHumansMetalloendopeptidasesReceptors, EndothelinAspartic Acid EndopeptidasesEndothelin-1Endothelin-Converting EnzymesEndothelin Receptor AntagonistsEnzyme InhibitorsMetalloendopeptidasesReceptors, Endothelin

Identifiers

PMID17965745
PMCPMC2275436
OpenAlexW2105356761

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.