Evidence map›Paper›PMID 30291906›Full record

ReviewPharmacology & therapeutics2019

Endothelins in inflammatory neurological diseases.

Pedro D'Orléans-Juste, Oscar B Akide Ndunge, Louisane Desbiens, Herbert B Tanowitz, Mahalia S Desruisseaux

Open access · greenAbstract readReview
In one paragraph

Review in Pharmacology & therapeutics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

30 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Astrocytic ET-1 System Determines Microglia Phenotype Following Spinal Cord Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. BQ788 reveals glial ETBritish journal of pharmacology · 2023
    Article
  17. Review
  18. Article
  19. Review
  20. Canadian journal of physiology and pharmacology · 2022
    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

5 authors at 3 institutions in 2 countries.

Pedro D'Orléans-JusteDepartment of Pharmacology, Faculty of Medicine and Health Sciences, Université de Sherbrooke, Sherbrooke, Quebec, CA, USA.
Oscar B Akide NdungeDepartment of Medicine, Yale University School of Medicine, New Haven, CT, USA.
Louisane DesbiensDepartment of Pharmacology, Faculty of Medicine and Health Sciences, Université de Sherbrooke, Sherbrooke, Quebec, CA, USA.
Herbert B TanowitzDepartments of Medicine and Pathology, Albert Einstein College of Medicine, Bronx, NY, USA.
Mahalia S DesruisseauxDepartment of Medicine, Yale University School of Medicine, New Haven, CT, USA; Departments of Medicine and Pathology, Albert Einstein College of Medicine, Bronx, NY, USA. Electronic address: mahalia.desruisseaux@yale.edu.
Albert Einstein College of Medicine · USUniversité de Sherbrooke · CAYale University · US

Funding

T. cruzi: pathogenesis modulation by eicosanoidsR01AI076248 · NIAID · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI TANOWITZ, HERBERT BERNARD · 2008 to 2012
$2.3M
Cerebral Malaria: Mechanisms of disease and neurological salvageR01NS069577 · NINDS · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI DESRUISSEAUX, MAHALIA S · 2011 to 2015
$1.8M
CIHR MOP-57883NIAID NIH HHS R01 AI076248NINDS NIH HHS R01 NS069577
6 · The paper itself

Abstract

Endothelins were discovered more than thirty years ago as potent vasoactive compounds. Beyond their well-documented cardiovascular properties, however, the contributions of the endothelin pathway have been demonstrated in several neuroinflammatory processes and the peptides have been reported as clinically relevant biomarkers in neurodegenerative diseases. Several studies report that endothelin-1 significantly contributes to the progression of neuroinflammatory processes, particularly during infections in the central nervous system (CNS), and is associated with a loss of endothelial integrity at the blood brain barrier level. Because of the paucity of clinical trials with endothelin-1 antagonists in several infectious and non-infectious neuroinflammatory diseases, it remains an open question whether the 21 amino acid peptide is a mediator/modulator rather than a biomarker of the progression of neurodegeneration. This review focuses on the potential roles of endothelins in the pathology of neuroinflammatory processes, including infectious diseases of viral, bacterial or parasitic origin in which the synthesis of endothelins or its pharmacology have been investigated from the cell to the bedside in several cases, as well as in non-infectious inflammatory processes such as neurodegenerative disorders like Alzheimers Disease or central nervous system vasculitis.

Indexed as

AnimalsEndothelinsHumansInflammationNervous System DiseasesEndothelinsBlood-brain barrier (BBB)Central nervous systemCerebral blood flow (CBF)ChymaseCytokinesEndothelin-1 (ET-1)Endothelin subtype A receptor (ET(A))Endothelin subtype B receptor (ET(B))Mast cells

Identifiers

PMID30291906
PMCPMC6348026
OpenAlexW2894906598

What OpenQuestion holds

Textmetadata
LicenceTDM
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.