ArticleCurrent cardiology reports2002
The role of endothelin in the pathogenesis of heart failure.
Article in Current cardiology reports, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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.
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.
Who cites it
3 citing papers in PubMed, 16 citations in OpenAlex.
- Role of Vasoactive Hormone-Induced Signal Transduction in Cardiac Hypertrophy and Heart Failure.Cells · 2024Review
- Cardiac biomarkers: new tools for heart failure management.Cardiovascular diagnosis and therapy · 2012Review
- Vasodilators in the treatment of acute heart failure: what we know, what we don't.Heart failure reviews · 2009Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In fewer than than 15 years since its discovery, endothelin is now recognized as playing a central role in the pathogenesis of chronic heart failure. This review examines the signaling pathways and mechanism of action of endothelin in relation to the studies that have elucidated this role. Early investigations observed that the endothelin system is markedly upregulated in heart failure, whereas others demonstrated that endothelin is the most potent vasoconstrictor. However, it has multiple other actions, including mediating pathologic hypertrophy and fibrosis of both ventricular and vascular tissues, acting as a proarrhythmic, and potentiating the effects of other neurohormones. Endothelin receptor antagonists were developed to investigate the hypothesis that these adverse effects could be prevented and experimental studies showed promise in this regard. Clinical studies to date have not fulfilled this promise. Further analysis of these trials will hopefully provide insight into these disparate findings and guidance for future investigations.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.