Evidence map›Paper›PMID 30657897›Full record

ArticleEuropean heart journal2019

A novel role for myeloid endothelin-B receptors in hypertension.

Alicja Czopek, Rebecca Moorhouse, Léa Guyonnet, Tariq Farrah, Olivia Lenoir, Elizabeth Owen, Job van Bragt, Hannah M Costello, Filippo Menolascina, Véronique Baudrie and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in European heart journal, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.5field-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

21 citing papers in PubMed, 44 citations in OpenAlex.

  1. Review
  2. Endothelin-1 signaling in the kidney: recent advances and remaining gaps.American journal of physiology. Renal physiology · 2025
    Review
  3. Dual ETFundamental & clinical pharmacology · 2025
    Article
  4. Review
  5. Article
  6. Article
  7. Mechanisms of lung endothelial cell injury and survival in pulmonary arterial hypertension.American journal of physiology. Lung cellular and molecular physiology · 2024
    Review
  8. Article
  9. Observational
  10. Immune and inflammatory mechanisms in hypertension.Nature reviews. Cardiology · 2024
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. The varying roles of macrophages in kidney injury and repair.Current opinion in nephrology and hypertension · 2020
    Review
  20. 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

15 authors at 5 institutions in 2 countries.

Alicja CzopekBHF Centre for Cardiovascular Science, The Queen's Medical Research Institute, University of Edinburgh, 47 Little France Crescent, Edinburgh, UK.
Rebecca MoorhouseBHF Centre for Cardiovascular Science, The Queen's Medical Research Institute, University of Edinburgh, 47 Little France Crescent, Edinburgh, UK.
Léa GuyonnetParis Cardiovascular Research Centre - PARCC, Institut National de la Santé et de la Recherche Médicale (INSERM), Paris, France.
Tariq FarrahBHF Centre for Cardiovascular Science, The Queen's Medical Research Institute, University of Edinburgh, 47 Little France Crescent, Edinburgh, UK.
Olivia LenoirParis Cardiovascular Research Centre - PARCC, Institut National de la Santé et de la Recherche Médicale (INSERM), Paris, France.
Elizabeth OwenBHF Centre for Cardiovascular Science, The Queen's Medical Research Institute, University of Edinburgh, 47 Little France Crescent, Edinburgh, UK.
Job van BragtBHF Centre for Cardiovascular Science, The Queen's Medical Research Institute, University of Edinburgh, 47 Little France Crescent, Edinburgh, UK.
Hannah M CostelloBHF Centre for Cardiovascular Science, The Queen's Medical Research Institute, University of Edinburgh, 47 Little France Crescent, Edinburgh, UK.
Filippo MenolascinaSchool of Engineering & SynthSys, Institute for Bioengineering, Centre for Synthetic and Systems Biology, University of Edinburgh, Edinburgh, UK.
Véronique BaudrieParis Cardiovascular Research Centre - PARCC, Institut National de la Santé et de la Recherche Médicale (INSERM), Paris, France.
David J WebbBHF Centre for Cardiovascular Science, The Queen's Medical Research Institute, University of Edinburgh, 47 Little France Crescent, Edinburgh, UK.
David C KluthMRC Centre for Inflammation Research, The Queen's Medical Research Institute, University of Edinburgh, 47 Little France Crescent, Edinburgh, UK.
Matthew A BaileyBHF Centre for Cardiovascular Science, The Queen's Medical Research Institute, University of Edinburgh, 47 Little France Crescent, Edinburgh, UK.
Pierre-Louis TharauxParis Cardiovascular Research Centre - PARCC, Institut National de la Santé et de la Recherche Médicale (INSERM), Paris, France.
Neeraj DhaunBHF Centre for Cardiovascular Science, The Queen's Medical Research Institute, University of Edinburgh, 47 Little France Crescent, Edinburgh, UK.
University of Edinburgh · GBThe Queen's Medical Research Institute · GBInserm · FRParis Cardiovascular Research Center · FRCentre for Inflammation Research · GB

Funding

British Heart Foundation FS/11/78/29328British Heart Foundation FS/13/30/29994
6 · The paper itself

Abstract

aimsHypertension is common. Recent data suggest that macrophages (Mφ) contribute to, and protect from, hypertension. Endothelin-1 (ET-1) is the most potent endogenous vasoconstrictor with additional pro-inflammatory properties. We investigated the role of the ET system in experimental and clinical hypertension by modifying Mφ number and phenotype. METHODS AND

resultsIn vitro, Mφ ET receptor function was explored using pharmacological, gene silencing, and knockout approaches. Using the CD11b-DTR mouse and novel mice with myeloid cell-specific endothelin-B (ETB) receptor deficiency (LysMETB-/-), we explored the effects of modifying Mφ number and phenotype on the hypertensive effects of ET-1, angiotensin II (ANG II), a model that is ET-1 dependent, and salt. In patients with small vessel vasculitis, the impacts of Mφ depleting and non-depleting therapies on blood pressure (BP) and endothelial function were examined. Mouse and human Mφ expressed both endothelin-A and ETB receptors and displayed chemokinesis to ET-1. However, stimulation of Mφ with exogenous ET-1 did not polarize Mφ phenotype. Interestingly, both mouse and human Mφ cleared ET-1 through ETB receptor mediated, and dynamin-dependent, endocytosis. Mφ depletion resulted in an augmented chronic hypertensive response to both ET-1 and salt. LysMETB-/- mice displayed an exaggerated hypertensive response to both ET-1 and ANG II. Finally, in patients who received Mφ depleting immunotherapy BP was higher and endothelial function worse than in those receiving non-depleting therapies.

conclusionMφ and ET-1 may play an important role in BP control and potentially have a critical role as a therapeutic target in hypertension.

Indexed as

Angiotensin IIAnimalsDisease Models, AnimalEndocytosisEndothelin-1HumansHypertensionMacrophagesMiceReceptor, Endothelin AReceptor, Endothelin BAngiotensin IIEndothelin-1Receptor, Endothelin AReceptor, Endothelin BEndothelinHypertensionMyeloid cell

Identifiers

PMID30657897
PMCPMC6396028
OpenAlexW2909113474

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.