Evidence mapPaperPMID 29637419Full record

ReviewCurrent hypertension reports2018

The Endothelin System: A Critical Player in the Pathophysiology of Preeclampsia.

Joey P Granger, Frank T Spradley, Bhavisha A Bakrania

Abstract readReview
In one paragraph

Review in Current hypertension reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
8.7field-weighted citation impact, top 2% 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

34 citing papers in PubMed, 83 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. The uteroplacental circulation at high altitude: adaptation and maladaptation.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025
    Review
  5. Article
  6. Observational
  7. Review
  8. Preeclampsia as a Study Model for Aging: The Klotho Gene Paradigm.International journal of molecular sciences · 2025
    Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Foetal lipoprotein oxidation and preeclampsia.Lipids in health and disease · 2022
    Review
  17. Article
  18. Article
  19. 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

3 authors at 2 institutions in 1 country.

Joey P GrangerCardiovascular-Renal Research Center, University of Mississippi Medical Center, Jackson, MS, 39216, USA. jgranger@umc.edu.
Frank T SpradleyCardiovascular-Renal Research Center, University of Mississippi Medical Center, Jackson, MS, 39216, USA.
Bhavisha A BakraniaCardiovascular-Renal Research Center, University of Mississippi Medical Center, Jackson, MS, 39216, USA.
University of Mississippi Medical Center · USState Street (United States) · US

Funding

STRUCTURAL VASCULAR ADAPTATION OF THE MICROCIRCULATIONP01HL051971 · UNIVERSITY OF MISSISSIPPI MEDICAL CENTER · 1993 to 2005
$11.3M
Tracking and Evaluation CoreU54GM115428 · UNIVERSITY OF MISSISSIPPI MED CTR · 2025 to 2025
$3.6M
Project 003 - Lorena AmaralP20GM121334 · UNIVERSITY OF MISSISSIPPI MED CTR · 2025 to 2025
$2.6M
Hypertension and Cardiorenal Research Training ProgramT32HL105324 · UNIVERSITY OF MISSISSIPPI MED CTR · 2025 to 2025
$819k
NHLBI NIH HHS P01 HL051971NHLBI NIH HHS R00 HL130577NHLBI NIH HHS R01 HL108618NHLBI NIH HHS T32 HL105324NIGMS NIH HHS P20 GM104357NIGMS NIH HHS P20 GM121334NIGMS NIH HHS U54 GM115428
6 · The paper itself

Abstract

purpose of reviewPreeclampsia (PE) is a disorder of pregnancy typically characterized by new-onset hypertension and proteinuria after gestational week 20. Although preeclampsia is one of the leading causes of maternal and perinatal morbidity and death worldwide, the mechanisms of the pathogenesis of the disorder remain unclear and treatment options are limited. Placental ischemic events and the release of placental factors appear to play a critical role in the pathophysiology. These factors contribute to a generalized systemic vascular endothelial dysfunction and result in increased systemic vascular resistance and hypertension. RECENT

findingsThere is increasing evidence to suggest that endothelin-1 (ET-1) in the maternal vascular endothelium is a critical final common pathway, whereby placental ischemic factors cause cardiovascular and renal dysfunction in the mother. Multiple studies report increased levels of ET-1 in PE. A number of experimental models of PE are also associated with elevated tissue levels of prepro-ET-1 mRNA. Moreover, experimental models of PE (placental ischemia, sFlt-1 excess, TNF-α excess, and AT1-AA infusion) have proven to be responsive to ET type A receptor antagonism. Recent studies also suggest that abnormalities in ET type B receptor signaling may also play a role in PE. Although numerous studies highlight the importance of the ET system in the pathogenesis of PE, further work is needed to determine whether ET receptor antagonists could provide an effective therapy for the management of this disease.

Indexed as

EndothelinsEndothelium, VascularFemaleHumansHypertensionIschemiaPlacentaPre-EclampsiaPregnancyEndothelinsBlood pressureCardiovascularEndothelinEndotheliumHypertensionPlacentaPreeclampsiaPregnancyVascular smooth muscle

Identifiers

PMID29637419
PMCPMC6064647
OpenAlexW2797873868

What Socratic 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 Socratic graph.